Welcome, everyone, to the 44th Annual J.P. Morgan Healthcare Conference. My name is Tess Romero, and I'm one of the Senior Biotech Analysts here at J.P. Morgan. Our next presenting company is Prime Medicine, and presenting on behalf of the company, we have CEO Allan Reine. Allan, over to you. Thank you, and thank you for having us at the conference today. Today, I'll be making some forward-looking statements, so please see our documents on file with the SEC. So I'm very excited to be here today to talk about Prime Medicine. Our technology, Prime Editing, I believe, has the potential to impact millions of patients' lives as we think about going into the future. This is based on a couple of things. One, I believe gene editing, which is really an early technology as we think about it, is going to be a very important tool as we look to human disease even today, but as we look out into the years to come. And Prime Editing really is the most versatile way to manipulate the genome. So this technology can do everything that any other gene editing technology can do, but also many other additional types of edits. That's because we can really write into the genome any sequence that we choose, so with that, we can do large deletions, we can do large insertions, we can do what we call hotspot editing, missense mutations, transversion mutations, so it's really an endless possibility of the types of diseases that we can ultimately treat with this technology. It's not only the most versatile way to edit the genome, but it's also the safest way to edit the genome, so we don't cause a lot of the consequences that you get with earlier gene editing approaches. We think there's a lot of important changes that are happening on the regulatory framework that we see today, so we think there'll be the ability to really move these therapies both faster and cheaper as we go into the clinic and ultimately to commercialization. We've got an extremely strong IP position around this technology that we've won exclusively in license from the Broad and that we've expanded on internally as a company. And we've already shown some clinical data that we put out last year that I'll share again with you today to show this really has curative potential in patients. So today, we're really strategically delivering on the promise of this. So how are we doing that? We're very focused today on our in vivo programs. So we have our liver franchise, and we're really executing on both Wilson disease and alpha-1 antitrypsin deficiency. And we have INDs for both programs coming this year. We have initial efforts underway. How do we expand beyond just these programs within our liver franchise? I think there's a lot of exciting, very large indications, even non-orphan indications, where Prime Editing offers a very differentiated approach that we can think about, and we hope to share more about that as we get throughout the year. BD is going to be a very important component on how we think about this therapy. So as we think about delivering on the promise here, how do we get this into more patients? We're not going to be able to do all of this alone. So doing more business development deals is going to help to expand the reach of this very important technology. Now, this is going to be an important year for the company as we think about 2026 and 2027. So the name of the game right now is focus. Let's get our programs into the clinic, and let's get towards proof of concept clinical data. So, for Wilson disease, we're planning for an IND or CTA in the first half of this year, and clinical data for that program, proof of concept clinical data for that program, in 2027. For our second liver franchise program, alpha-1 antitrypsin deficiency, we're planning for an IND and/or CTA in the middle of this year, again with proof of concept clinical data coming in 2027. Our third program is in cystic fibrosis. That program, we continue to make good progress. There's a tremendous unmet need in patients that either can't tolerate or are not amenable to current standards of care. That'll be the initial low-hanging fruit that we plan to go after here. Ultimately, we believe we can treat the majority of that population, and we hope to share some additional in vivo proof of concept data for that program in 2026. As you look at our pipeline today, what you see is a pipeline really focused on high-value programs. So what defines a high-value program for Prime Medicine? A high-value program is a program where we think there's a high probability of success, high probability of technical success, there's a near-term clinical endpoint that can show a proof of concept in that disease, and there's a large addressable market. Large, I'll put in quotations, but it's relatively large as we think about orphan diseases. And I'll go into the patient populations here and explain why these are multi-billion-dollar opportunities. So that's where our focus is today. But again, the plan is to expand that as we build this company and think about other areas where we can get a lot of synergy into what we want to do next. We're continuing to make good progress as well with our BMS collaboration. There we collaborated. We signed a collaboration deal at the end of the third quarter in 2024. That's based on ex vivo CAR T therapies for both oncology, hematology, and immunology. There's some pretty significant also preclinical milestones that come as part of that transaction, and there was $110 million upfront when we signed that deal. So that's sort of one deal that we're doing, but there's going to be, we hope to be more as well. And again, the idea is how do we expand the reach of this really important technology. Here's the clinical data that I alluded to earlier. So this is in a disease called chronic granulomatous disease. And we've shared this data. It's in the New England Journal of Medicine now, which was published late last year. It essentially is showing you that we functionally cured two patients. This is an ex vivo therapy, so we're manipulating hematopoietic stem cells and then giving those sort of back to the patient. They're in grafting. It's very quick engraftment, and you're seeing a very impressive set of data here. We are in discussions, and we're trying to figure out a way to bring this to patients and potentially more to come there. As we think about the off-target, what I alluded to before in terms of what differentiates this technology even beyond the versatility and what we can do with it, is the safety. This is some of the data that we had generated as part of our CGD program. You can see here we have no detectable double-strand breaks. We have no detectable off-target edits, no detectable bystander edits, as you shouldn't expect that with Prime Editing. We don't see detectable deletions, chromosomal rearrangements. And oftentimes, we actually use CRISPR-Cas as a positive control here. And we've recapitulated this data for really a number of all of our lead programs as well. So this is, again, I'll emphasize the safest way we believe to edit the genome. Now, we're building this platform to really optimize modularity. So how can we quickly go from program to program? How can we quickly go from mutation to mutation even within the same disease? And I want to hone in here on a couple of things. So one is the regulatory frameworks. So how has that changed over the last six months to a year? It's the ability, and I think we've heard the FDA or other companies state this, the ability to do multiple mutations with the same disease under one IND. I think we've received some feedback that we believe will allow that to go forward. I even think the European regulators are also starting to pay more attention here, and we hope we see some progress there where there's an allowance there as well. We recently received some feedback that we're going to be able to leverage some of our IND enabling studies for Wilson disease for our alpha-1 antitrypsin program. Why is that? As you think about drug product, when we look at our liver-directed programs, we're using the same lipid nanoparticle. So the only things that are really changing here are slight changes to the sort of cargo as we think about these three squiggly lines you see in the middle, right? The majority of that drug product stays the same. And that is really what likely is going to dictate safety and other things. So the ability to kind of leverage from one program to the next, again, is a tremendous amount of savings and time as we think about going from mutation to mutation within a disease, going from disease to disease within the same tissue. And again, this is an incredible amount of synergy, and we're really excited to be able to leverage there. And I do want to talk a little bit about our intellectual property that we have around this technology. So just to make it clear, any combination or permutation of a CRISPR-Cas enzyme, a template guide RNA with a reverse transcriptase, is Prime Editing. Full stop. You can call it something else. You can put a fancy name to it. That's still Prime Editing. And I can assure you we're going to very vigorously defend and enforce our intellectual property at the right time. So turning to our liver franchise, so I mentioned before, these are large opportunities for orphan indications. They're two of the largest genetic diseases. For Wilson disease, we believe there's about 10,000 patients in each of the U.S. and the E.U. Japan actually potentially has a higher prevalence rate, so there could be 7,500 patients plus. So as we think about this disease globally, there's a significant number of patients and a significant commercial opportunity. We're not going to go after 100% of these patients because we can't go after every mutation. So as we think about the U.S. European market, we think with a handful of editors, we can probably get to about, or in the U.S., Europe, and Japan, we can probably get to about 25,000 or so patients just with six editors or the six most common mutations. There's also potentially an incidence rate here of 300 patients per year. So it's not just kind of treat that area under the curve, but the question is, how do you actually build a long-term business here as you think about some of these indications? Then for alpha-1 antitrypsin deficiency, that's a population of about 10,000-15,000 patients as you think about the U.S. and Europe, so call it 20,000-30,000 patients within those geographies. That tends to be more of a sort of Caucasian disease, so there's not as much of a global opportunity. But again, 99% of those patients are going to have the same mutation. So you can essentially go after all of those patients with one drug product with one editor. So to talk a little bit about our data in Wilson disease. So this is showing on the left panel here our two lead mutations that we're going after. So the first one we plan to bring to the clinic in the first half of this year is the H1069 editor. You can see we're getting very high levels of editing efficiency here. We're getting similar high levels of editing efficiency with our second mutation we're planning to progress, which is the most prominent mutation in the Asian population, and there again, we're getting well above 80% editing efficiency. You could see here, as I mentioned before, we don't see any off-target editing in any of our programs, and you could see that here on the right where we're really only editing that dot you see above the gene that we're trying to edit. We're not seeing anything from an off-target standpoint. From a preclinical phenotypic side, so what happens when we actually make this edit with high efficiency, well, as you look at the middle panel here, the left is wild type. The middle shows what an untreated mouse looks like that has the H1069Q mutation. On the right is a mouse with that H1069Q mutation that has then been treated with our editor. On the left and on the right, you could see we've essentially normalized hepatic copper concentration. We are mobilizing that copper out of the liver, which is what repairing that enzyme or correcting that enzyme should do. Copper is typically excreted through the fecal route. In patients that have these mutations, you get copper buildup in the liver. It ultimately goes into the blood, and you get very high urinary excretion and very low fecal excretion. We're essentially showing here that you can normalize that fecal excretion. We also have data that shows that urinary excretion also goes down, so that's being normalized as well. It's almost a full phenotypic rescue, but as I say, sort of a picture. You could see it in a picture. And here you can see on the left is sort of that wild type mouse. And this is what's called a copper challenge or radiolabeled copper challenge. So you're giving these mice radiolabeled copper. In the middle, you can see that liver, that yellow that's just lighting up. All that copper is accumulating in the liver because they don't have this enzyme to be able to excrete it normally. And on the right is that treated mouse, which looks identical almost to wild type. So you're getting almost full restoration of hepatic copper. So we are also going to be doing radiolabeled copper PET in the clinic. So this will be an important clinical endpoint in addition to a lot of other kind of biomarkers that you can look at for Wilson disease to allow us to get to sort of proof of concept data again in 2027. As we think about our clinical plan here, as I stated, we're going to start with H1069Q as sort of the first mutation. That's about 30%-50% of the population in the U.S. and Europe. The second will be R778L, which is the most predominant Asian mutation. And then we have a handful of other editors to sort of get to those percentages of the population that I mentioned before. And this is a disease that standard of care really hasn't changed in decades. The KOLs that we've talked to, and we did a big KOL event internally at AASLD, there's a lot of excitement to get to a drug that can impact these patients' lives. They have to be on low copper diets. They've got to take lifelong therapy with iron chelators and zinc salts that these docs would love to get these patients off of. This is a very exciting therapy, and we look forward to bringing that into the clinic. For alpha-1 antitrypsin deficiency, the goal here is to really normalize alpha-1 levels in humans. You could see here patients that are homozygous for what we call the Z mutation have very, very low levels of this enzyme at baseline. The goal is, how do we get these patients back to normal? What we show here is very high levels of editing efficiency. In the middle, you see here it shows the amount of corrected protein in the blood versus mutated protein. You could see at the higher dose level, we're almost completely normalizing the levels of M protein in the blood and essentially taking in these mouse models all the way back to the normal range. So beyond Alpha-1 and Wilson, I just want to talk a little bit about what our plan is in terms of business development again. So I think there's a number of areas that we're looking at. So one is, what can we do sort of within our core, some of the programs that we have today? And I think there's a lot of excitement as we think about our current pipeline. There are going to be things that we want to do outside of our core, and there's a lot of interesting areas to take this technology. One example of that is what we've done with BMS, but I think there's a lot of other ways we can capitalize on what we're doing beyond just this ex vivo CAR-T with BMS. And there's a lot of interesting things we're thinking about there. Two examples I've listed is neuro diseases and other areas within cell therapy, and there's also delivery technology. So how do we ensure, as the field progresses, that we're taking advantage of delivery? So as delivery to the brain advances and delivery to other tissue types, we think we've got the best cargo. So as technologies advance, we'll let other companies trailblaze there, but we want to ensure that we're taking full advantage of that de-risking that others are doing, and hopefully, some of this we can also do with partners today. So in closing, look, this is a big year for the company, as I've said. Getting our first two in vivo programs into the clinic is going to be an important milestone for us and really drive towards proof of concept data as we look into 2027. As I mentioned before, as we think about business development in other areas to really broaden the reach of this technology, we're really laser-focused on that execution and excited for the year. And with that, I'll sit down for some questions. Great. Thanks, Allan, for the presentation. So I thought I would start with a little bit of a bigger picture question here. I mean, I think last year, from what I understand, you had a very extensive pipeline that you were moving forward, and you've sort of refined the focus in these two areas. What were the kind of key pushes and pulls of making those decisions and thinking that was the best path forward for the company? And then we'll dive into some specific questions. Yeah, no, that's a really good question. So I joined the company in January of 2024. I actually think I came to J.P. Morgan, but I was joining a week later and did meetings with Prime. So I think it was announced. I was allowed to do that. And when I joined, there were about 18 programs in the pipeline. So we knew we weren't going to be able to take all of those programs forward on our own. But one of the first things that I did with the company is, let's do a full strategic review. We called it a value framework exercise. And let's evaluate every program. We took about three to four months. We involved a lot of people across the company and really focused on some of the things I mentioned in my presentation, like what's the commercial opportunity? What's the potential chances of how do you handicap success in the clinic? What is the timeframe to clinical data, right, so there were some indications, like some ocular indications that we were exploring. We had really good preclinical data, but we could have been four-to-five years before we got to a proof of clinical concept data set. We looked at technical feasibility, so do delivery technologies exist today that we have high confidence in that we can explore, and obviously, what's the patient population? What's the unmet need? There's additional parameters beyond that, but we did work essentially on all of those and kind of ultimately kind of what rose to the top, and for our liver franchise, we know that editors, at least we've seen it done already with CRISPR, and we've seen it done now with base editing, that you can deliver safely to hepatocytes. So there we saw there's a high probability of technical success. There are areas where we think prime editing can be differentiating. So for Wilson disease, they're predominantly what are called transversion edits. So other gene editing approaches won't work there. So that's somewhere where really only prime editing could do. So that sort of became obvious. And for alpha-1 antitrypsin deficiency, although it's somewhat of a more competitive market, I believe that prime editing is the best approach for that disease. Taking that patient or that gene completely back to wild type, I think, is what will win out in the end of the day there. So that was sort of how we kind of those are some ideas of how we did that exercise. Cystic fibrosis is another one. So there we're working hard on sort of delivery to the lung. And the Cystic Fibrosis Foundation is predominantly funding that program. And we are making good progress there. And obviously, BMS and other things that we're doing. So that's sort of how the exercise went and kind of where we got our focus from. And I think it's allowed us to move quickly now into the clinic soon with two programs and really create a company that we think can create significant value for patients and for shareholders over the next couple of years. Okay. And Allan, from a regulatory standpoint, you talked about some of your kind of key themes or key takeaways that you see for the overall space in terms of how the agencies are thinking about gene editors. We did notice this IND and/or CTA for both of your programs. Can you just help us better understand what you mean by that and why it's an and/or? Yeah, I think about it more as an and than an or. We usually use the and/or because the and/or is sort of what's going to happen first. So we're not necessarily defining that. These are both, if you think about Wilson disease and alpha-1 antitrypsin deficiency, these are going to be global studies. So this is not just going to be an IND. There's always the thought of what's going to go first. We haven't commented sort of which is coming first. I would say for this, there's no reason you wouldn't do an IND before a CTA. I think this is really going to depend on where the patients, where the sites that we want to start with, etc. That might dictate kind of what gets opened up first. Okay, and can you touch a little bit on, for those that might not be familiar, the IP estate you have across the portfolio, including the foundational IP for the platform, including a number of the Prime Editing technologies? Yeah. So again, we've got, I think, six U.S., 12 global patents that really cover both the foundational IP, many different iterations of Prime Editing because there's sort of the initial Prime Editing. There's a lot of changes that have happened along the way. And so as I think about the IP, we've got an umbrella that covers, as I said before, anything that has to do with a Cas enzyme, a reverse transcriptase, and a guide, right? That is Prime Editing. And anyone that's doing anything just using those components is infringing on our IP. So we've got very broad coverage there. Obviously, as you dig a level deeper, there's a lot of other innovations within Prime Editing that we also cover that others couldn't do. But even if they're just doing something with those components, that's going to infringe on our foundational IP. Other changes they might make might infringe on other things that we also have patented. I think that's why we've been able to receive this IP on our sort of foundational technology where others have sort of tried and been able to get sort of that foundational IP issued. Companies can often get IP issued on specific products, right? That's going to happen. They might infringe a broader patent estate, but you can get product IP that'll ultimately infringe on our IP. And so there are companies out there that don't have any foundational IP behind it but do have product, may have product IP issued or filed that may or may not get granted. And they are, and we believe, will be infringing, and we will vigorously defend our IP in the future and enforce. Just in terms of the PM577 program, it seems like it's a huge focus for you guys in getting this into the clinic here. What are the gating factors at this point? Yeah, I mean, we're not commenting on sort of where we are. We've just said the filing is going to happen in the first half of this year. So if we start to talk about gating items, then we tell you exactly the playbook and where we are. What I would say is for any IND, you need to get through all your IND enabling studies, your GMP manufacturing, and you've got to write an IND, which is no small task, which is many, many thousands of pages, and ultimately submit. So what I'd say is we remain on track and have made good progress and expect a regulatory submission in the first half of this year. So sorry, I can't answer it directly, but that's the best answer I can give. Yeah, I had to try. I had to try. Okay. And with that in mind, when do you think, if all goes according to plan, you'll be able to initiate your phase one trial or phase one two trial, rather? And what is your latest thinking around the design? Yeah. So for initiation, as soon as your regulatory submission is "accepted," then it's just getting sites up and running, and that can take a month or two, getting through IRBs, etc. So typically, you'll see with most companies, enrollment will start two months to maybe three months post getting the regulatory submission accepted. So that's how I think about the start date based on when we announce that that regulatory submission has been accepted. In terms of trial design, as you said, there's a phase 1/2 trial. Phase 1/2 trials, by design, you're going to assess safety. So it'll be a dose escalation trial that's looking at safety predominantly. But these are gene editing programs, right? Gene editing has tended to have really strong translation as you've gone from animal to human. And so we're looking at diseases where we believe there are good biomarkers that are going to allow us to see very early on if we're having the desired effect. So you can see very early in these studies, you can get to clinical proof of concept, I believe, very early in the diseases that we're looking at. So for Wilson disease, that dose escalation, as I mentioned before, we're going to be doing copper PET in some of these patients. So what you visualize with those models that we're kind of turning around that 360, we'll be able to show that in patients that we're getting that copper clearance. And we're not going to mandate in every patient, but potentially, you'll be able to see that from a dose-dependent manner kind of what happens in people. We'll be looking at other endpoints there as well. You can look at fecal copper, urinary copper. Some of the patients will get liver biopsies. You can look at hepatic copper. You look at something called ceruloplasmin levels as well, which are impacted, which don't change on standard of care. Ultimately, the goal is going to be to remove standard of care and show that these patients' copper balance stays normalized even with the removal of standard of care because that's the ultimate goal for these patients. Okay. Okay. And Allan, it sounds like as part of your kind of strategic review that you did last year, you thought about kind of like, "Okay, how long does it take to get from IND or CTA to being a commercial product?" So can you give me a little bit of a framework for Wilson disease or an archetype of how you think about that from a broad strokes basis? Yeah. Look, I can give you a broad strokes basis. I think it's all data dependent. I think what gene editing drugs can do is very different than what we've seen historically. So if it translates that you can get very high levels of editing efficiency, what does that mean? Well, that means I've taken a patient that has a mutation. And let's say I can do 100% editing efficiency. I'm not saying what we're going to do. But let's say it was 100% editing efficiency in the cell types you wanted to get to. Well, now 100% of those cells are producing normal protein, and they're under what we call endogenous control, so normal physiologic control. You're turning on that enzyme when it needs to be turned on, and you're getting the right amount of that enzyme produced at the right time, right? That's really powerful. It's a powerful technology that we're looking at, so I think as we think about endpoints, if this translates into humans and we can do in animals what we can, if we can translate that data in animals to humans, we can get high levels of editing efficiency, then those things should be normalized, and so as you think about the regulatory paradigm and what that could look like, I think that lends itself to potentially doing smaller studies and to potentially getting to endpoints, biomarker endpoints that can really kind of dictate how these patients will do over time, so I can't give you sort of a timeframe of what we can do to commercial because it is going to be data dependent. But if this translates how we believe it'll translate, I think there'll be many opportunities to move fairly fast from a phase 1/2 to registration to commercial. What is your view of the evolving development landscape in Wilson's? Anything you have an eye on, or do you think you're really taking forward a pretty premier ideal approach here? So I think this has the potential to be a best-in-class therapy. And I haven't seen any other approaches that I think will really compete with the profile that I think we can achieve in patients. However, I want to be clear, we're not going to be able to treat 100% of Wilson patients. So if we can get to 60-ish plus% in the U.S., that's 40% of the patient population that can get other therapies. Call it in Asia, maybe there'll be 40% in the U.S. and 30% in Asia that can get other therapies. So there'll be room for other therapies. I know there's a gene therapy that's being developed. Not to get into sort of what I think the differences are, but I do think a gene editing approach could be far superior here to what a gene therapy approach can do. I think there's some other kind of novel chelators that are coming along, which won't have a dramatic change on the disease or the course of the disease. It may offer something that's a little bit more less dosing and other things, but won't be a dramatic change to the course of the disease. So I don't see anything out there that I think can really compete with what this drug could do if it gets commercialized. Okay. Okay, great. And then just for the sake of time, let's maybe move to PM647 for AATD. Why do you think you have an ideal approach here for the treatment of AATD? And what overall product profile do you think would be compelling for a one-time prime editor? And in turn, what could that market penetration look like given how competitive the space is? Yeah. I mean, so the different approaches out there, there are RNA editors that have reported some data. And we'll get more data and higher doses over time, and we'll see how that changes. But at least what we've seen to date, I don't know that those will be competitive. They are going to be chronically delivered drugs. So they're not one-and-done therapies. But we'll see how that data develops over time. I think there's three programs at least that I know of or three companies that are working on that. There's Beam with a base editing program, and I think they've demonstrated some pretty promising data showing that they can get sort of those alpha-1 levels to what I would call sort of the heterozygote level or the carrier level, which tend to be fairly. I think those patients tend to be normal and don't have disease. So if they can sort of maintain that, that could be a drug there. There are some differences. The base editing approach, they do have a bystander edit in the majority of the edited protein. So there's always going to be a question if that changes any of the functionality of that protein. I think what we've seen is functional protein, but there'll always be that question that kind of hangs out there. And as we look at the Prime Editing approaches, there are two other companies that are doing Prime Editing. So I think, as I've said before, that we believe that's Prime Editing. And I do believe Prime Editing can be the superior approach here because, again, you're taking that mutated protein exactly back to wild type. There are no other changes. It is the normal protein. And we hope we'll be able to get to levels that can be higher within the carrier range or even within the normal range. So I do believe the Prime Editing approach will be the winning approach over time here in this disease. With any novel technology, there are key risks. So Allan, what keeps you up at night about what you're doing at Prime? I sleep pretty well for the most part. But as I look across the company, I do think there's a responsibility here in terms of this really is an incredible technology, right? I believe that. That's why I joined the company. I think this is a technology I said at the beginning. It sounds like a provocative statement, but I really think this can impact millions of people across the world. I really believe that. And so what keeps me up at night is, are we doing the right things? Are we making the right decisions? Are we shepherding this technology in the right way to make sure it gets to enough patients, it gets to people throughout the world? That's sort of what gets us excited to go to work every day, but also kind of what keeps you up at night. Am I making the right decisions? Am I doing the right things? There's no doubt in my mind the value of this technology, right? So given the value of the technology, we've got to make sure it succeeds in the right way and make the right decisions to make that happen. Okay. And you talked a little bit about how your archetype or your framework for how you think about business development for the company. It sounds like maybe something with the CGD program could be near term. What do you think is most priority for 2026? Yeah. I wouldn't think about CGD in terms of BD. I think the patient population there is too small. I think if we were going to do something with CGD, that'd be something Prime can do on our own to try and create some value there. Oh, I see. And what do you mean by that exactly? Is there a way to get even to talk to regulators or a way to get approval even with a couple of patients? And how you want to think about that is, is there some way to create some value with that program internally? So that's stuff we're doing some work on. There's nothing more that I can share today, and we'll see how that goes. But I wouldn't think about that as anything for business development. I think it's just too small of a product. Okay. Okay. So for 2026, the kind of framework that you outlined, it had a lot of parts to it. So what do you think 2026 is actionable this year? Yeah. I mean, look, I don't like to put timeframes on anything with BD because these things can take longer or shorter, obviously, depending. So who knows when things get done? But look, again, I think this technology is now a reality, right? We've treated two patients. We've basically cured two patients. We're going to be in the clinic with in vivo therapies. We'll be de-risking as we go. There are so many other areas where this technology should be developed today that, frankly, if we had endless capital, we would think about some of those things. So doing that with partners, I think, is important. So again, I think cell therapy is really exciting. I think neurological disease is really exciting. I think there's other areas that we're excited about. I think additional liver indications is really exciting where we see even, as I stated before, potentially very large indications. So again, we never make promises with BD, but I think given where we're going and what we're doing, I'm hopeful we'll get something done. Okay. Okay, great. Last question for me is just I'm actually going to ask how much cash do you have, but it looks like it's on the slide in front of me. So it sounds like $227 million. Can you just orient us to what the key milestones that allows you to get through? Key milestones? Yep. From your cash runway. Oh, cash runway. So I think the key milestones as we think about this year and we haven't said exactly when the cash runway is in 2027, but for this year, it's getting our two programs into the clinic. I think those are key. We didn't talk about it. We have an arbitration going on with Beam. So we expect resolution of that sometime in the first half of this year, which I think is an important milestone to get through. For our cystic fibrosis program, it's getting to really prove a concept. Preclinical data there, I think, is important. Obviously, BD can serve as milestones as well, both new BD deals potentially, but also within our BMS collaboration, there's pretty significant milestones, $185 million in milestones. So being able to achieve one of those is a possibility as we think about our current cash runway. And we haven't said when in 2027 we're ultimately going to have data. So I can't sit here definitively today and say this current cash runway gets us through that, although that depends. But there are some of these non-dilutive things that can happen as well that help us get through that. Okay. Well, I think this might be a good place to leave it. I want to thank Allan and the Prime team so much for being here and doing this presentation with us. And thanks to all the listeners for joining as well. Thank you. Thank you for having us. Thanks. Thanks. Okay. Thanks. Okay.