Brian D. Gibson - Principal Financial Officer, Chief Accounting Officer, Vice President of Finance, Corporate Secretary and Treasurer Dominick C. Colangelo - Chief Executive Officer, President and Director Ronnda L. Bartel - Chief Scientific Officer

Chad J. Messer - Needham & Company, LLC, Research Division Stephen G. Brozak - WBB Securities, LLC, Research Division Kaey T. Nakae - Ascendiant Capital Markets LLC, Research Division Jason Kolbert - Maxim Group LLC, Research Division

Ladies and gentlemen, thank you for standing by, and welcome to the Aastrom Biosciences First Quarter 2013 Conference Call. [Operator Instructions] I would like to also remind you that this call is being recorded for replay. I will now turn the conference over to Brian Gibson, Aastrom's Vice President of Finance. Brian D. Gibson: Thank you, Tyrone, and good afternoon, everyone. Welcome to our first quarter 2013 conference call to discuss our most recent financial results and the progress of our development programs. Before we begin, let me remind you that on today’s call, we will be making forward-looking statements covered under the Private Securities Litigation Reform Act of 1995, and all of our projections and forward-looking statements represent our judgment as of today. These statements may involve risks and uncertainties that are described more fully in our filings with the SEC, which are also available on our website. In addition, any forward-looking statements represent our views only as of today and should not be relied upon as representing our views as of any subsequent date. With us on today's call are Aastrom's President and Chief Executive Officer, Nick Colangelo; our Chief Scientific Officer, Dr. Ronnda Bartel; and our Chief Business Officer, Dan Orlando. We are also pleased to have a special guest speaker with us Dr. Nabil Dib, a world-renowned interventional cardiologist and Director of Cardiovascular Research at Mercy Gilbert and Chandler Medical Centers in Phoenix, who will discuss his participation in Aastrom's Phase IIb I xCELL-DCM clinical trial. Following our prepared remarks, we will open the call to your questions. I will now turn the call over to Nick. Dominick C. Colangelo: Thank you, Brian, and good afternoon, everyone. Since our fourth quarter conference call in March, we've taken several important actions to advance our company and the development of our lead product candidate, ixmyelocel-T. But first, we implemented an R&D strategy focusing our clinical efforts and resources on our dilated cardiomyopathy, or DCM, orphan disease program, which we believe provides a streamlined path to commercialization for ixmyelocel-T and represents a substantial commercial opportunity for Aastrom. Second, we enrolled and treated the first patients in the ixCELL-DCM study, which is now well under way at a number of U.S. clinical sites. The objective of this study is to evaluate the efficacy and safety of ixmyelocel-T in the treatment of patients with advanced heart failure due to ischemic DCM. Dr. Dib will share his perspective on the urgent medical need for these heart failure patients and the potential use of ixmyelocel-T in this indication in a few minutes. Third, we filed an S-1 registration statement to sell $25 million of common stock in a fully marketed follow-on offering to support the Phase IIb DCM clinical program and other corporate activities. We believe that this is the most appropriate structure in timing for the financing, as a successful offering will provide the capital required to complete the ixCELL-DCM study and obtain the data supported -- to support advancing the program into Phase III clinical testing. In focusing on the development of ixmyelocel-T to treat advanced heart failure due to ischemic DCM, we're targeting an area of major unmet medical need in a highly compelling commercial opportunity for ixmyelocel-T. Heart failure remains a leading global health issue. Approximately 5.5 million people in the U.S. suffer from heart failure and there are an estimated 550,000 new cases in the U.S. each year. Medical costs to treat these patients now total more than $25 billion annually and this figure is expected to more than triple over the next 20 years. DCM, which is characterized by weakening of the heart muscle, enlargement of the heart chambers and an inability to sufficiently pump blood throughout the body, is the third leading cause of heart failure and the leading cause of heart transplantation. A majority of the advanced heart failure patients, who are refractory to medical therapy, which is more than 0.25 million patients in the United States, have DCM and approximately 60% of these cases are of ischemic origin due to atherosclerotic cardiovascular disease. These patients typically have maximized their use of prescription and device therapies and are no longer candidates for further revascularization procedures such as angioplasty and bypass surgery. At this stage of the disease, they have very limited treatment options, including placement of left ventricular assist devices, or LVADs, and heart transplantation. This is a well-defined patient population at a well-defined point-in-disease progression, which makes these patients optimal candidates for treatment with ixmyelocel-T. There's also a strong preclinical and clinical rationale for developing ixmyelocel-T in this indication. Preclinical results have demonstrated that ixmyelocel-T significantly and reproducibly reduced cardiac tissue damage and had additional cardioprotective effects in relevant disease models. Further, our Phase IIa clinical results demonstrated that ixmyelocel-T was well tolerated in patients with DCM and that consistent positive efficacy trends were observed in ischemic DCM patients treated with ixmyelocel-T. Finally, we believe that the refractory ischemic DCM market represents a significant commercial opportunity for Aastrom for several reasons. In addition to a growing patient population, we have a leading position in this indication and an opportunity to make ixmyelocel-T the first approved product for the treatment of ischemic DCM. We also have a potentially streamlined regulatory pathway based upon ixmyelocel-T's U.S. orphan drug designation for this indication and a strong for pharmacoeconomic rationale to support premium pricing based on the limited availability and high cost of treatment involving LVADs and heart transplantation for these patients. To tell us more about the treatment of these patients with advanced heart failure due to ischemic DCM and the rationale for testing ixmyelocel-T in this indication, I'm pleased to introduce Dr. Nabil Dib, Director of Cardiovascular Research at Mercy Gilbert and Chandler Medical Centers in Phoenix; Associate Professor of Medicine and Director of Clinical Cardiovascular Cell Therapy at the University of California, San Diego; and founder and editor-in-chief of the Journal of Cardiovascular Translational Research. Dr. Dib is a world-renowned interventional cardiologist and a principal investigator in the ixCELL-DCM study. Dr. Dib?

Well, thank you, Nick, for your nice introduction. As an interventional cardiologist with more than 15 years of clinical trial experience in the treatment of advanced cardiovascular disease, as an investigator in the ixCELL-DCM trial, I am very pleased to share my perspective on the unmet medical need in the treatment of patients with advanced heart failure and the therapeutic potential of ixmyelocel-T to treat these patients. As Nick indicated, there are currently very limited treatment options for patients with advanced heart failure due to ischemic cardiomyopathy -- we call it DCM -- which is extremely frustrating for patients' family and their health care professional. That biggest challenge for these patients is the market loss in what's called exercise capacity, which really refer to daily living activities such as shopping for grocery or walking from the car to the stands to watch a grandchild's ballgame and so on. As Nick mentioned, for patients who can no longer benefit from medical therapy, devices such as pacemaker or further revascularization procedure such as angioplasty, the only remaining current treatment option are ventricular assist devices or heart transplants. And as you know, the heart donors are so scarce. Even in the United States alone, there's only about 2,800 transplants per year. Fortunately, for these patients, early study results from promising cell therapy like ixmyelocel-T indicate strongly that we may be able to fill this gap and restore living capacity for many of these patients. I choose to be an investigator -- am honored to be an investigator in this clinical trial, of the ixCELL-DCM trial, because I have the significant amount of research on the use of cell therapy to treat advanced heart failure. And I find that ixmyelocel-T, which is a compromise of multiple key effector cells, such as mesenchymal stromal cells and M2-like macrophages, have tremendous therapeutic potential and make it a unique product in the market of cell therapy. The data from Aastrom Phase II studies suggest that ixmyelocel-T can deliver benefit in patients who have very few treatment alternative. I am compelled to help these patients as a physician. And as a researcher, I am committed to the advancing science in the area of great unmet medical need, which will bring me to my final reason for participation in this study. I like the trial design of the Phase IIb trial. The ixCELL-DCM study is well designed to demonstrate definitive and meaningful clinical results. The primary outcome of mortality, hospitalization and heart failure, ER visit, emergency room visits, plus the secondary clinical, functional and symptomatic efficacy measure are the type of meaningful clinical endpoint that the regulatory agency, FDA, and medical community are looking for. I only choose to be part of the trial that I feel are well designed to have the opportunity to make a significant contribution to medical practice and benefit patients. Dominick C. Colangelo: Thank you, Dr. Dib, for sharing your insights and perspective. We greatly appreciate your comments, and we'd ask that you remain on the call for any questions from our listeners at the conclusion of our prepared remarks. As we reported last month, enrollment in our Phase IIb ixCELL-DCM study has begun and we've treated our first patients in the study. The ixCELL-DCM study is a multi-center randomized, double-blind, placebo-controlled Phase IIb study designed to evaluate the efficacy and safety of ixmyelocel-T in patients with advanced heart failure due to ischemic DCM. The study is designed to enroll 108 patients with advanced heart failure at approximately 30 clinical sites in the U.S. and Canada, with the primary endpoint being the number of all-cause deaths and hospitalizations and unplanned emergency room visits for IV treatment of acute worsening heart failure over 12 months. We will also be evaluating several secondary clinical, functional and symptomatic efficacy measures at 3, 6 and 12 months. As previously communicated, we expect to enroll the study by the end of Q1 2014 and to have top line efficacy results from the study in Q2 2015. We believe that Aastrom is well positioned to execute the ixCELL-DCM study for several reasons. First, as I mentioned earlier, the target patient population for the study, advanced heart failure patients refractory to medical therapy, is well defined in a distinct point in disease progression with limited treatment options. Second, our targeted investigators, interventional cardiologists, routinely perform catheter-based procedures and coordinate with heart failure specialists in the management of patient care. Our study sites, which are concentrated in areas of high disease prevalence, are experienced in using the NOGA MyoStar catheter system for cell therapy studies as that system is specifically designed for cell therapy delivery. And finally, we believe that 30 sites -- study sites in the U.S. and Canada should be sufficient to enroll 108 patients, according to our current study time lines. Turning to our R&D efforts, we mentioned on our last conference call that ongoing research by Aastrom scientists and our collaborators continues to define the highly differentiated mechanism of action of ixmyelocel-T and the broad therapeutic potential for Aastrom's platform and products. Results of some of this research has been presented at important international scientific meetings over the past few weeks, and I'd like to turn the call over to our Chief Scientific Officer, Dr. Ronnda Bartel, to briefly review some of these important findings. Ronnda? Ronnda L. Bartel: Thank you, Nick. As mentioned, ixmyelocel-T stands up from other cell therapies because its primary effective cells include not only mesenchymal stromal cells, or MSCs, but also M2-like macrophages, a cell type that plays a key role in tissue repair and generation that is not found in other cell therapies. M2-like macrophages are known to play a beneficial role in atherosclerosis, providing clear support for our effort to investigate the impact of ixmyelocel-T on the underlying pathology of coronary artery disease. As some of you may already know, atherosclerosis is characterized by both in accumulation of cholesterol and chronic inflammation of the vessel lining, or endothelium, which together lead to the formation of plaque in vessel blockage. To test the hypothesis that ixmyelocel-T could address these 2 hallmarks of atherosclerosis, we conducted animal studies and presented results over the past few weeks at the 19th Annual International Society for Cell Therapy and the Atherosclerosis, Thrombosis and Vascular Biology 2013 Scientific Sessions. The poster and presentation, which can be found on Aastrom's website, report that ixmyelocel-T may help address the issue of cholesterol accumulation via the M2-like macrophages. These cells were shown to actively take up modified cholesterol, acetylated low-density lipoproteins, or LDL, and transfer this cholesterol to both apoA-I and high-density lipoproteins, or HDL, which is the first steps in removing excess cholesterol. In addition, when cholesterol-loaded ixmyelocel-T was administered to animals, the cholesterol was shown to accumulate in the serum and liver of the animals and it was eventually excreted, the normal route of elimination of cholesterol. Other data presented focused on the impact of ixmyelocel-T on other aspects of atherosclerosis, namely the endothelial dysfunction caused by chronic inflammation. When added to endothelial cells, ixmyelocel-T increased nitric oxide production, an important vasodilator, and also endothelial nitric oxide synthase, or eNOS, the enzyme responsible for making nitric oxide. Ixmyelocel-T also reduced oxidized stress by reducing the levels of reactive oxygen species and increased the amount of the antioxidant enzyme superoxide dismutases in activated endothelial cells. In addition, ixmyelocel-T reduced endothelial cells inflammatory markers such as ITM-1, VTM-1 and MCP-1, while increasing the very important anti-inflammatory cytokine, Interleukin-10. These effects were also associated with the reduction in apoptosis, or death of endothelial cells. The combination of M2 macrophage activity with the cholesterol-transport activity positions ixmyelocel-T as a highly promising and appropriate investigational therapy for patients with advanced ischemic DCM. Dominick C. Colangelo: Thank you, Ronnda. At this time, I will turn the call over to Brian Gibson for his brief financial report before opening the call for questions. Brian D. Gibson: Thanks, Nick. For the first quarter ended March 31, 2013, Aastrom had a net loss attributable to common shareholders of $6.8 million, or $0.15 per share, versus $9.7 million, or $0.25 per share, for the same period in 2012. The change in net loss reflects the noncash changes in the fair value of our warrants and the noncash accretion of the convertible preferred stock. Our loss from operations for the quarter, which excludes the impact of the warrants and preferred stock, was $7.2 million, or $0.16 per share, compared to $8.6 million, or $0.22 per share, a year ago. Research and development expenses for the quarter ended March 31, 2013, were $5.5 million versus $6.8 million for the same period a year ago. The decrease in R&D expense was primarily attributable to the reversal of nearly $900,000 of noncash stock-based compensation expense, related options forfeited as a result of the corporate restructuring announced in March. The remainder of the decrease was primarily due to lower purchasing and manufacturing supplies to align inventory levels with the expected clinical production volume. General and administrative expenses for the first quarter ending March 31, 2013, were $1.6 million versus $1.8 million for the same period in 2012. This decrease is primarily attributable to the reversal of noncash, stock-based compensation expense related to the corporate restructuring. At the end of the quarter, Aastrom had $9.2 million in cash and cash equivalents compared to $13.6 million at the end of 2012. Our cash use for operations of $6.8 million during the quarter was in line with our previous forecast of $6.5 million to $7.5 million and was partially offset by nearly $2.4 million in net proceeds from our ATM during the quarter. We expect our Q2 cash spend to be in the $4.5 million to $5 million range, as we ramp up enrollment in the ixCELL-DCM trial and continue to execute cost-cutting measures as part of the restructuring. As for our financing plans, and as Nick mentioned earlier, we filed a form S-1 registration statement with the SEC last week to sell up to $25 million in stock. Earlier this week, the SEC informed us that the filing would not be reviewed and, therefore, we are kicking off the formal offering process now. I can't comment on the specific timing for closing on the transaction at this point. However, we do expect to have the process completed by the end of the second quarter. We believe the proceeds from this financing will provide approximately 2 years of additional cash, funding the company beyond ixCELL-DCM data in Q2 2015. That completes my review of the financials, and I'll now turn the call back to Nick. Dominick C. Colangelo: Thanks, Brian. I believe we've taken the right steps to address our capital requirements and improve our financial position as we advance ixmyelocel-T for the treatment of advanced heart failure due to ischemic DCM. We're now in a much stronger position to execute our Phase IIb ixCELL-DCM study, prepare for Phase III testing and consider other potential indications for ixmyelocel-T. This concludes our prepared remarks. Now I'd like the operator to open the call to your questions.

[Operator Instructions] Our first question is from Chad Messer of Needham & Company. Chad J. Messer - Needham & Company, LLC, Research Division: This one is for Dr. Dib. You mentioned the Phase II data, the -- I guess, the Phase IIa data on DCM and, of course, as an early proof-of-concept trial, it was small and uncontrolled and didn't tab the kind of functional outcome that we're going to get now in the Phase IIb. But as you look at that data, I was wondering if you could just walk us through what in there was most encouraging to you and do you think is most predictive of the potential success in the current trial? Brian D. Gibson: Dr. Dib?

Yes, I'm sorry, I was on silence, I guess. Do you hear me now? Brian D. Gibson: Yes, we can hear you. Did you hear the question?

Yes, I do not have here exactly the slide in front of him. Do you have those slides? Are you asking about a specific question or just the result in general? Chad J. Messer - Needham & Company, LLC, Research Division: It's pretty open in general. I'm wondering what in that data you found that gave you -- you said the data was encouraging to you and I'm wondering if you could comment on specifically what you found most encouraging in it.

Yes. Now in general, if you look at the 13 years of stem cell therapy experience, the most important finding in clinical -- I'm sorry, in the stem cell therapy, a very modest improvement in the objective findings, like ejection fraction and so on, is very modest. And I think here, the clinical benefits is probably have the most value for the patients -- from patient point of view, their improvement in their physical activity, as well as the goal here is to concentrate on rehospitalization, which is probably one of the most beneficial for patients and for the health care in terms of cost-effectiveness, as well as a clinical endpoint. If you look at all what they look for, in general, they do look at the hospitalization, quality of life and mortality. And all that exists in a positive direction in this -- in the Aastrom product.

The next question is from Steve Brozak of Web Securities. Stephen G. Brozak - WBB Securities, LLC, Research Division: This is actually Steve Brozak from WBB, but this question is for Dr. Dib as well. Your expertise is actually in trial design and the outcomes. And based on that, can you walk us through, not so much in the past what you've seen, but how you see this trial design being differentiated, basically, in terms of what you look to see and what would be positive outcomes into the future?

Yes. And I can speak very highly for this design of the clinical trial comparison to other trial that has been done. And the most powerful thing in this design of clinical trial, in addition to the good design, in terms of double-blind trial, in terms of randomization that the clinical endpoint that this trial is looking for, and this really one of the most -- that's what differentiates this trial from other clinical trial we have done, specifically for heart failure. And here, as you see, we are looking for a clinical endpoint that relates to a quality of life of the patient and more important, to their hospitalization, rehospitalization. This is a very critical and important clinical endpoint, for patient is important, for health care industry important. You can imagine if we decrease the rehospitalization of patients. For sure, we decrease -- improve their quality of life and for sure, we -- or most likely, will affect their survival, but also very important for the health care in terms of cost effectiveness. You can imagine how much we can also improve on the cost effectiveness for health care. And that's why I think that will pay very important role in terms of the reimbursement in the future for cell therapy. Stephen G. Brozak - WBB Securities, LLC, Research Division: I'll end it one -- with one last question. Given the fact that you do -- you did have training at Harvard on trial design, you also, obviously, are very capable in assessing wherewithal in finances on trials. Given the fact that, obviously, you got to put together a trial, you're looking at a system now that the trial, the trial design and the resourcing for that trial is something that you now are comfortable with for Aastrom going forward. Would that be an accurate statement?

That will be an accurate statement, yes.

Our next question is from Kaey Nakae of Ascendiant Capital. Kaey T. Nakae - Ascendiant Capital Markets LLC, Research Division: My question is for the Aastrom scientist who was speaking earlier. You gave us some insight about the ability of the product as it relates to atherosclerosis. I'm wondering if you can give us any further insights about the product as it relates to ischemic tissue repair and that being any effect on angiogenesis or formulation of the right type of cardio cells that are needed to increase the functionality of the heart? Ronnda L. Bartel: Okay. This is Ronnda. We have demonstrated in animal models that we do see an increase in tissue perfusion with the treatment of ixmyelocel-T, the -- we see cardiac remodeling, we see increase in thick -- wall thickness around the infarct areas. So we've seen aspects of all of that in our animal studies, so I'm not sure if that answers your question or not. Kaey T. Nakae - Ascendiant Capital Markets LLC, Research Division: Well, I guess what I'm trying to get to is in terms of some of the improvements that we've seen with some of the other trials using stem cell therapies for heart failure, the effects don't seem to be all that durable, so I'm wondering, is there anything specific that you believe about your science that could lead to better outcomes? Ronnda L. Bartel: Yes, I think it's because the -- we've seen structural changes in the tissues and that tends not to be a transient issue. But the major thing for me is that differentiates this from the other studies that were done, is the presence of macrophages because it really is a -- it's not just MSCs or bone marrow mononuclear cells, it incorporates those things as well as the M2 macrophages, so it's kind of a broader approach to treating the indication.

Our next question is from Jason Kolbert of Maxim Group. Jason Kolbert - Maxim Group LLC, Research Division: And so, Ronnda, can we just pick up where you left off, what is it about the M2 macrophages that they're producing that you're run-of-the-mill or highly selective homogeneous population of MSCs wouldn't produce? Ronnda L. Bartel: Well, to me, I don't think there's a lot of factors that are necessarily different, but it's the cell-related activities. You've got phagocytosis, efferocytosis, you -- the remodeling capabilities with extracellular matrix that you don't see with the other cell type. Plus, it's in the context of the other bone marrow cells and the MSCs. Jason Kolbert - Maxim Group LLC, Research Division: Okay, fair enough. And so I'd like to drop back in little bit and talk about ischemic DCM. Dr. Dib, when a patient comes in, what's the entry criteria for this patient? How do you qualify them of an ischemic etiology? And how do you decide what level of DCM that they're actually experiencing? We're all familiar with CLI, where we were trying to select the sweet spot between a Rutherford 4 and a Rutherford 5 patient. Is there a similar grading system in DCM that you're using to select patients that will get the most benefit but that are not so far gone that maybe won't get -- won't be able to be helped?

Yes, extremely important question, extremely important question. And the way we select those patient, depending on a clinical symptoms, number one. And number two, depending on objective finding, testing that we do. For the clinical symptoms, we have a classification depending on New York heart class, so it will be Class 1, 2, 3 and 4. And 4 is the worst and 1 is the best. And usually, those patients in category 3 and 4, which means on minimal activity, even if they are walking in the room, they might have shortness of breath. Sometimes, if they are sleeping, they wake up with shortness of breath. That's the clinical symptom that's usually. So minimal activity can induce their symptoms. Fatigue, tired, short of breath, those are the complaints. Now we go and we always look ischemic versus non-ischemic is easy to differentiate. If patient have heart attack in the past we call them ischemic, or if they have significant blockages in the blood vessel of their heart, decreasing the blood flow to the heart, those are ischemic. Now we go farther and say, if we cannot fix those artery with a stent, everything usually done for those patients, they already -- if bypass surgery can be done, it should be done, if angioplasty or stent can be done, it should be done. And usually those patient, they have all those already done and they have some of them a pacemaker already in place and they are on optimal medical therapy, which is beta-blockers, ACE inhibitors and so on. But despite the standard of care and that's what's really the importance of this -- of the biologic and cell therapy in this field. So in addition to standard of care, all standard of care there, and they are exhausted and patient continue to suffer, those are the patient -- and angiographically if nothing can be done for them and their heart function reduced less than 30% their function by echocardiography and, well, of course, we'll look at some criteria just to make sure that the procedure is safe, which just means that the aortic valve is okay. We cut across it, there's no clot in the heart, in the ventricle. So is it safe, per se? Those are the patient that surely we would like to -- will be the ideal candidates for this. And from my experience, I did the first stem cell therapy in the United States with the myoblast and it was a Class 3 and 4 population. And we don't want to cross the line to go to a very, very sick patient, who is taking inotrope and his heart is very sick, he might not tolerate the procedure and we can increase the risk. We can have complication that can lead to a problem. So, yes, there is a fine line and very important to recognize a clinically and with objective testing to make sure that we can do the procedures safely and we can -- hopefully, they will help -- also benefit from the cell therapy in the same time. And those are not small number of patient. As you know, in the United States alone, there's 500,000 patients per year die of heart failure and actually, 2/3 of them is ischemic, between 65% to 70%. Those are ischemic because of a coronary artery disease. There's a 5 million admission per year from heart failure. And 2/3 of those, as I said, ischemic. So the market is huge in terms of the market. But for us, for the clinical trial, we have to clearly train our investigators to do that safely. Like what you said, there's a really good fine line between safety and efficacy. Jason Kolbert - Maxim Group LLC, Research Division: And just remind me, how did you come to the decision to use NOGA mapping versus delivering to multiple arterial branches via what may or may not be the infarct-related artery? It just seems like it would be a simpler, faster procedure. What's the benefit that you're getting in NOGA and how will that compare or comparatively compare across different DCM patients?

Yes, another very important question in the cell therapy world. And I was part of the NOGA mapping development since 1998, when I was in Harvard and after that. I get the first stem cell approval using the NOGA mapping for the gene in the year 2002 and then 2004 for the myoblast, the stem cell myoblast, so we worked very hard on this. Now what's the rationale behind giving the cell direct injection versus intracoronary? Found in many studies that the retention rate of the cell are different in the chronic setting than the acute setting. And when I say chronic setting, meaning the heart failure population versus acute myocardial infarction population. So you -- when you talk about the recent heart attack or just somebody have a heart attack, you hear that they gave the cell inside the artery. But when you hear about heart failure, you see they did direct injection, because the cytokine and the inflammatory process and the environment is different between patients with acute myocardial infarction versus heart failure patients. So we expect the retention rate to be better with direct injection versus giving intracoronary. Now if this product showed to be very beneficial in the acute myocardial setting, and I think they will expand in the future towards acute myocardial setting, then that would be another -- that will be the clinical indication where you can deliver this therapy intraarterially. As a matter of fact, I am designing catheter myself for intracoronary delivery and it's just like catheter going this [indiscernible] mark. But again, here specifically because of a heart failure, the inflammatory process is different and we think the retention of the cell to be better with the direct injection with the NOGA mapping. Jason Kolbert - Maxim Group LLC, Research Division: Perfect. Great answers. My last question comes back to Ronnda. And it's just can you remind us on the math on the Phase II clinical trial? How did you come to the patient number and how do you talked it all about what the powering -- statistical powering assumptions are behind this trial, as well as the monthly enrollment assumptions around the number of sites you've selected? Dominick C. Colangelo: Yes, Jason, I'll start there. First of all, the trial is powered to show -- at 80%, to show a reduction over 12 months from 1.7 events to 1.1 event in the drug-treated group. In terms of enrollment, at this point, we've said that we expect to complete enrollment in the study by the end of Q1 2014. Obviously, we're kind of in early days of the study, having just started treating patients. Generally, it's not standard practice for management teams to provide frequent interim updates on at-site activations and patient enrollments and so we don't plan to do that. We certainly will follow that practice and only provide updates on our projected enrollment completion time line if and when it's warranted. But for now, as I mentioned, we expect to complete enrollment by the end of Q1 2014.

There are no further questions at this time, I'd like to turn the call over to Mr. Colangelo for any closing remarks. Dominick C. Colangelo: Okay. Well, thank you, Tyrone. And again, I'd like to thank Dr. Dib for joining us today and the thank our callers for your questions and continued interest in our company. And I look forward to updating you on our next call. Thank you very much.

Ladies and gentlemen, thank you for your participation in today's conference. This concludes the program. You may now disconnect. Have a wonderful day.