Good morning, ladies and gentlemen. Welcome to the Cellectis live conference call, English session. At this time, all lines are in a listen-only mode. Following presentation, we will conduct a question- and- answer session. If at any time during this call you require immediate assistance, please press star zero for the operator. This call is being recorded on Monday, September 14, 2026. I would now like to turn the conference over to Arthur Stril, CFO and CBO. Please go ahead. Good morning, everyone, and thank you for joining us. I am Arthur Stril, Cellectis' Chief Financial Officer and Chief Business Officer. Before we begin, please note that this presentation contains forward-looking statements within the meaning of applicable securities laws, including the Private Securities Litigation Reform Act of 1995, including statements regarding our strategy, development programs, financial conditions, and potential future prospects. These forward-looking statements are based on our current expectations and assumptions and are subject to various risks and uncertainties that could cause actual results to differ materially from those expressed or implied by such statements. For a discussion of these risks and uncertainties, please refer to our filings within the U.S. Securities and Exchange Commission, including, without limitation, our 6-Ks, annual report on Form 20-F, our press releases, and annual financial report prepared in French. Except as required by law, we undertake no obligation to publicly update or revise any forward-looking statements contained in this presentation. Here is our agenda and speakers for today. Dr. André Choulika, our Chief Executive Officer, and Dr. Adrian Kilcoyne, our Chief Medical Officer. We will walk you through Cellectis, a gene-editing company, our in vivo gene editing pipeline, followed by our strategic transformation. We'll then present our next steps and open the floor for your Q&A. I would now like to turn the call over to André. Thank you, Arthur. Good morning, everyone, and thank you for being here. I'm André Choulika, Co-Founder and CEO of Cellectis. What I want to share with you today is one of the most important updates in the history of this company. A deliberate, science-driven turn towards the next chapter of gene editing. I'll walk you through where we come from, where we're going, and why we believe this is the right moment to make this move. Let me start with a simple idea, the one that has defined this company for a quarter-century, gene editing. Cellectis was founded more than 25 years ago as a pioneer in this field, long before gene editing became a household term it is today. Our conviction has never wavered. Gene editing is not an incremental improvement in medicine. It's a paradigm shift. At its core, gene editing does one thing. It intervenes at the level of the genome to change how a gene behaves. You can do that in three ways. You can silence a gene, you can activate a gene, or you can repair a gene. Keep those three verbs in mind, silence, activate, repair. This is what it's going to be all about. Why does this matter so much? Because genetics drives diseases. Cancer, diabetes, obesity, neurological disorder, immune conditions, even the biology of aging. At the root, these are genetic variations in the genome. Aberrant gene expression, polymorphisms, genes doing too much or too little. The logic of gene editing is simple. Fix the gene and you fix the disease. Now, there are two ways to do that. Ex vivo, where we collect patient cells, edit them under controlled manufacturing conditions, and infuse them back. That's the world of CAR T, and it's the world where Cellectis built its leadership. In vivo, where we deliver the editor directly into the body to the target tissue and do the editing inside the patient. This is the pivot in one sentence. We're building on our ex vivo leadership to advance the next frontier in in vivo genetic. Same expertise, same molecular toolbox, delivered in a fundamentally simpler way. Let's talk about in vivo genetic and why I'm so excited about it. The liver is the chemistry lab of the human body, and conveniently, it's also the easiest address for a lipid nanoparticle to find. Everything you inject intravenously ends up passing through it. The concept is simple. A single intravenous injection, product travels to the liver, our editor does its work inside the liver cells, and the effect is designed to last. No apheresis, no manufacturing per patient, no hospitalization for cell collection and preconditioning. One injection for long-lasting effect. What exactly is the product? It's remarkably simple. It's a messenger RNA that encodes a gene editor. All base editor packaged inside the liquid nanoparticle, an LNP. It's a well-established, well-understood delivery technology. The messenger RNA is transiently expressed, it does its job and disappears. But the edit it makes in the genome is permanent. That's the elegance. One-time treatment, lasting effect, which brings me to the heart of today's news. We've made the decision to advance two preclinical candidates, both in dyslipidemia, diseases of blood lipids, where the genetic drivers are exceptionally well- understood. The first is.HEAL-101, targeting the APOC3 gene in severe hypertriglyceridemia. The second is.HEAL-201, targeting PCSK9 in severe hypercholesterolemia. Both are messenger RNA plus LNP products. Both go after targets that are exceptionally well-validated by other modalities, and both are designed around the same promise, a single IV injection with a potentially long-lasting effect..HEAL-101. This is gene surgery for severe hypertriglyceridemia. Severe hypertriglyceridemia doesn't get the headlines of cardiovascular diseases, but it should. These patients live with the risk of acute pancreatitis, a condition that hospitalizes you, is extremely painful, and can kill you. They carry elevated cardiovascular risk. The quality of life is poor, and their options are thin. 1 million- 2 million high-risk patients across the U.S. and Europe. Not a rare disease, but a neglected one, as APOC3 is a very small protein, hard to address with a drug. Here's the program we've built for them. Here's.HEAL-101 in a single frame. Severe hypertriglyceridemia at the high risk of pancreatitis. The target is APOC3. APOC3 has been validated twice over by other modalities. The technology is a TALE base editor that disables the gene. The goal is to make a single treatment with a durable triglyceride lowering. We have already obtained preclinical data strong enough that we are heading to the clinic. Let me explain how it works, because the mechanism is where our differentiation really shows..HEAL-101 is a base editor. Rather than cutting the DNA, which is how third-generation gene editing worked, it changes a single letter of the genetic code. A precise conversion of one base, the C to a T, at exactly the position we choose in the APOC3 gene. This is the key point for safety. There is no DNA break. We are not relying on the cell to repair a cut. We simply rewrite one letter. No double-strand break means the potential for cleaner, improved safety profile that matters enormously when you are treating patients in vivo. What does changing one letter accomplish? It creates a stop codon, a stop signal inside the gene. When the cell reads the gene, it now stops early. The full APOC3 protein is never made. In plain terms, we introduce one tiny, precise edit, and the gene that drives the disease is switched off. This is gene surgery. Here is the evidence. When we introduce.HEAL-101 into human liver cells, we see highly efficient editing right at the target site in the left panel. Just as important, look at the right panel. Across the top [quartiles] of target sites, we see essentially no modification. High on-target activity, high specificity. This is exactly the profile you want to see before moving into humans. The functional consequence follows directly. As we increase the dose of.HEAL-101, we see the frequency of disabling edit climb. In parallel, the secretion of APOC3 falls. Editing goes up, disease-driving protein goes down. The biology behaves exactly as designed. Then we move into humanized animal models, mice engineered with human liver cells, and we see the full chain of cause and effects in a living organism. Precise editing of APOC3, a clear decrease in the APOC3 protein, and the outcome that matters clinically, a real drop in triglycerides. The magnitude of that effect is what I want you to remember today. In affected mice, a single administration of.HEAL-101 produces a 70% reduction of APOC3 and a 76% reduction in triglycerides. 76% from one treatment. This is the kind of effect that can change a disease, not just manage it. Now to our second program,.HEAL-201, a slightly different, equally powerful type of gene surgery. The disease is severe hypercholesterolemia, high LDL cholesterol, or the so-called bad cholesterol. LDL is the leading driver for atherosclerotic cardiovascular disease, and we know that lowering it reduces cardiovascular events. Yet a large number of patients simply cannot get to goal, even on maximum-tolerated therapies. We focused on the highest need patients, younger, high-risk individuals who had a premature cardiovascular event and still have persistently elevated LDL despite everything available today. Again, roughly 1 million-2 million patients across the U.S. and Europe. Here is.HEAL-201 at a glance. The indication is severe hypercholesterolemia. The target, the PCSK9 gene, one of the most thoroughly validated targets in all cardiovascular medicine. The editing technology is different from the one I just showed. It is a TALE modulator that silences PCSK9. I'll come back to the silencing point later. The goal is one-time treatment for durable LDL lowering to reduce cardiovascular risk. Again, we've obtained promising preclinical data supporting moving this product candidate into the clinic. Here's what I want to highlight, the breadth of our platform..HEAL-201 works differently from.HEAL-101. It's not a base editor. It's an epigenetic modulator. It doesn't change a single letter of DNA at all. Instead, it binds the gene and silences it epigenetically, turning the gene off while leaving the DNA sequence completely intact. Think of it this way. With.HEAL-101, we edit a letter in the DNA. With.HEAL-201, we simply flip the switch to off without touching the text. Same company, same file backbone, two entirely different type of mechanism. That's what surreal gene editing platform look like. No DNA sequence change means, again, an additional safety rationale. The data backs it up. With an epigenetic change alone, no sequence modification, we shut down PCSK9 transcription completely. The messenger RNA of PCSK9 dropped to near zero. The gene is effectively turned off at the source. That translates to the protein. Over the days following treatment, PCSK9 protein secretion falls dramatically and stays down. The target protein is turned off, which is precisely what drives LDL cholesterol lower. Specificity is, of course, critical. So we looked across the entire transcriptome, every gene expressed in the cell. The result, PCSK9 is knocked down cleanly while the rest of the genome is essentially untouched in the expression. Gene surgery uses a scalpel, not a hammer. High specificity for PCSK9 and PCSK9 alone. Crucially, the effect is durable. This is the question everyone asks about epigenetic approaches. Does it hold? In biology, epigenetic pattern is stable over time, even over a lifetime. Our data show rapid and sustained decrease of PCSK9 that remains stable over time. Rapid onset with a lasting effect. This is exactly the profile a one-time therapy needs. When you will see the data, let me give you some timelines. I would like to turn the call over to Adrian to walk you through our clinical plan for.HEAL-101 and.HEAL-201. Adrian? Thank you, André. I will now outline our development pathway, which is composed of two parts. Initially, we have an accelerated path to first-in-human data through an investigator-initiated trial in China. This IIT is being run under the new regulations which came into effect in May this year, requiring a comprehensive preclinical package. This first-in-human study in severe hypertriglyceridemia is focused on safety, tolerability, and establishing that.HEAL-101 will lower triglycerides, which we have seen in the compelling preclinical data, some of which has already been shared today by André. It is important to highlight that parallel IND and CTA preparation is ongoing to allow for a seamless transition to the global phase I-B/II by end of 2027 in the target patient population. This will also inform the path to phase III. It is important to also recognize that the endpoint of lowering triglycerides is well- established as a surrogate endpoint for reduction in the risk of acute pancreatitis. There will be no requirement for a cardiovascular outcome trial for either approval or reimbursement. This has a significant impact on the path to revenues compared with many lipid programs. I will now show the plan for.HEAL-201. This plan follows the same strategic pathway as.HEAL-101. That is accelerated path to first-in-human data and seamless transition to global phase I-B/II trials. This phase I first-in-human study in severe hypercholesterolemia aims to establish safety and LDL-C lowering, followed by a phase I-B/II, which will focus on the highest risk population who would benefit most from a single-dose gene therapy offering durable, long-term lowering of cardiovascular risk. These include younger high-risk patients, patients with severe genetic hypercholesterolemia, patients with premature cardiovascular disease, and patients with persistent elevated LDL-C despite maximal therapy. It is important to highlight that LDL-C lowering is an established and validated surrogate endpoint that is accepted to support approval by both FDA and EMA, which, like.HEAL-101, will enable an efficient path to market. Overall, we believe we have designed clinical programs that offer an accelerated path to first-in-human data that will demonstrate the potential of a single-dose gene therapy to offer long-lasting efficacies in areas of high unmet need. Our anticipated timelines are outlined on the slide now being shown. For.HEAL-101, we expect the first patient to be treated in Q1 2027, with data readouts in the second half of 2027. It is important to highlight that early patients may demonstrate the expected durable responses by end of year, which could distinguish this as a product with best-in-class potential. As stated earlier,.HEAL-201 follows the same strategic pathway. We therefore anticipate that first patients will be enrolled in the second quarter of 2027. The first data readout is expected in the first half of 2028, with, again, early patients having the opportunity to demonstrate durable responses. In parallel, we continue to accelerate all activities, including IND and CTA-enabling activities with early engagement with the FDA and EMA. Our goal is also to ensure manufacturing is ready to support the demands of global supply. In summary, we have two first-in-human [inaudible] ready clinical programs with preliminary clinical data expected in the second half of 2027 and the first half of 2028, respectively. Each offers the potential to be best-in-class products with long-lasting efficacy in areas of significant unmet need. I would now like to turn the call over to André to present our world-class gene editing capabilities. Thank you very much, Adrian. Now, let me step back up to the platform because these two programs are just the first expression of something bigger. This is what sets us apart. Most gene editing company do one or two things. We have the full toolbox. With our TALE technology, we can act as a nuclease, as a base editor, as an epigenetic modulator, and as a transcriptional regulator..HEAL-101 uses the base editors..HEAL-201 uses the epigenetic modulator. The same core competency span across all columns. Let me make these advantages explicit because it is central. First, a broad toolbox. Nuclease gene editing, base editing, epigenetic editing, and transcriptional regulation. Any modality from one single platform. Second, strong differentiation at the molecular level. Our TALE editors bind DNA without nicking it with precision down to the base pair. The third, 32 base pair recognition site that gives us an exceptional specificity. Third, we can combine these tools for the same indication. Any modality, any hybrid combinations of them for safety, tools to finesse the biology of each diseases. This is a meaningful competitive advantage. Let's talk directly about the pivot, the strategic decision itself, and the discipline behind it. The hem onc landscape have changed, and it has changed for good reasons. In B-ALL, frontline blinatumomab consolidation has cut relapse rates from roughly half to 15%-25%. In NHL, cema-cel in frontline consolidation is driving deeper MRD conversions. Bispecifics and ADCs are crowding second line and third line, and there is now an in vivo CAR T rush in LBCL. In other words, patients are doing better earlier. That is unambiguously good news for medicine. It is also a smaller and more crowded pond for third-line plus therapies. But it changes the map for us. When relapses fall and competition rise, our enrollment slows, trial gets longer and more expensive, and the registration moves further into a more crowded market. Put plainly, the opportunity for lasme-cel and eti-cel has narrowed. We looked at this landscape honestly and asked ourselves where Cellectis can create the most value. The answer was clear. Here's the pivot laid out plainly. Cellectis today has lasme-cel in phase II and eti-cel in phase I. We're making the disciplined decision to exit the internal cell therapy program while continuing to support our existing partners program, which remains valuable. Cellectis tomorrow is an in vivo gene-editing company advancing.HEAL-101 and.HEAL-201 towards the clinic backed by our partnerships. This decision also extends our cash runway into the fourth quarter 2027 into the second half of 2028. We are concentrating our resources where the science, the medical need, and the value creation are the strongest. We're making four commitments. We accelerate our two lead in vivo gene editing assets with readouts.HEAL-101 with the first human readout in H2 2027 and.HEAL-201 with first human readout in H1 2028. We exit internal cell therapy development of lasme-cel and eti-cel. We continue our existing partnerships, AstraZeneca, Servier, Allogene, and Iovance, that the value doesn't go away. We realign the organization around in vivo gene editing and extend the cash runway into the second half of 2028. That's in vivo gene editing-focused company with a full year of financing past its first human readout. Which brings me to where we are heading and to a world you've seen through today..HEAL..HEAL is more than a program. It's our purpose. Gene surgery is editing life for the better. We're not leaving our history behind. We're fulfilling it. With in vivo gene editing, we have the immense opportunity to transform medicine at its source and make a paradigm shift in the way patients are treated a reality. I hope you'll be part of this next chapter with us. With that, let me thank you for your attention and open it up. Arthur, David, and Adrian are all here, so we can be ready to answer your questions. Thank you very much for your time. Ladies and gentlemen, we will now begin the question- and- answer session. If you would like to ask a question during this time, you have to press star then the number one on your telephone keypad. Again, that'll be star then the number one on your telephone keypad. If you want to withdraw your question, that'll be star then the number two. Your first question comes from Amin Makarem from Jefferies. Please go ahead. Hi, this is James on for Amin. Congratulations on the strategic transformation, and thanks for taking our question. For.HEAL-101, what would the program need to demonstrate to be meaningfully differentiated from existing APOC3-directed therapies, including antisense and siRNA approaches? Also, just another quick follow-up, for both 101 and 201 programs, what off-target biodistribution work, liver safety work has to be completed for each program, and what remains before the first patients could be dosed? Thanks. Well, thank you very much, Amin, for these questions. I would like to turn the first question to Adrian and the second part of your question probably to David for all the preclinical work and before getting into the clinic. Adrian? Yeah, thanks, Amin, for the question. As you have seen from the preclinical data, we get very strong efficacy. We would expect our efficacy is at least as good as existing therapies. The really important differentiator for us is really based on the gene editing that is safe but also very durable. We think one of the challenges, we have done market research on this, we have talked to many cardiologists, endocrinologists, et cetera, those involved in treating these patients, and they have identified a group of patients that they will feel would benefit significantly from a very durable patient. We have outlined those in the slides, which are those younger patients. But it is really that durability of response. Of course, the level of durability remains to be seen, but there is every anticipation that this will be a very long-lasting effect. For young patients with significant cardiovascular risk or indeed patients with severe hypertriglyceridemia who run the risk of developing acute pancreatitis, the ability to not have to have repeated treatments for the rest of their lives is very attractive to clinicians and to patients. I think really the importance is the safety of our gene editing technology and the potential for very significant durability of effect. In terms of the off-target, I will hand over to you, David. One of the things I would like to add to your question, Amin, here is while ASO, RNAi, et cetera, these are not long-term therapies. They can be lasting for a certain period of time, but the problem with most of these diseases is adherence of the patient to the treatment. That is where the problem comes from. When you have no real symptoms and you have to take pills on a daily basis, even on a weekly or monthly or sometimes on three months' basis, it is complicated for certain patients, especially when they are young, especially when they have no symptoms, et cetera. Gene surgery is like the surgery concept. People prefer to have one definitive action in order to fix a problem instead of continue to go after the sentence. I think that this is something that where the medicine of 21st century is going to head at in the coming years, and intervention on the genome is going to become one of the big changes where people will stop taking pills. As for example, normal surgery has changed the lives of a lot of patients in term of certain type of treatments also. David, I would like to turn off the hold for you. As for assessing off target, we do that at two different levels. We assess the off target at the molecular level for the TALE-based editor and TALE epigenetic modifier. These are pursued essentially in a way that is quite similar to what we have made public for the TALEN, with a systematic, unbiased approach, so we know where the strike will take place, and we are pretty sure that it does only what it is supposed to do. The off-tissue approach is essentially assessed through biodistribution studies made in animal models, and we actually pursue not only the detection of the lipid nanoparticle itself, the lipids, but also the payload and any effect thereof. This essentially, a succession of models that have been classically used in the field, and we are going to pursue the same, and we are pursuing the same path. Got it. Thank you for taking our question. Your next question comes from Jack Allen from Baird. Please go ahead. Great. Thanks for taking the questions and congratulations on the updates. I guess, two quick ones from our end. The first is around the proof of concept data that we are going to get as early as the second half of next year from.HEAL-101. How do you think about dose escalation here, and what kind of dose you could potentially enter the clinic? Do you expect the initial doses to be effective doses, and what kind of proof of concept data could we expect as it relates to breadth and depth of that data set in the first second half of next year? Then I have a quick follow-up as well on the delivery mechanism. Okay. Thank you, Jack. Great question. Maybe Adrian can. We've worked a lot on the dose, and I know that you've done tons of work with the physicians. Adrian, please go ahead. Yeah, indeed. It's a great question, Jack. Thanks for asking it. It's really important to us that we start as an effective dose. I think our preclinical work has demonstrated very reassuring safety and tolerability. The group we're working with has done extensive modeling to enable us to start at a higher but safe and effective dose. When we talk about dose escalation, we anticipate we're already starting at a relatively effective dose. We would anticipate that the initial emerging data will also be giving us some strong safety signals. Yes, we may have to dose escalate, but it'll be far probably less than we might have anticipated. I think this extensive modeling, with a center that has extensive experience in these type of therapies, is allowing us to have that higher starting dose. Got it. Do you have any context around what that dose might be as it relates to milligrams per kilogram? Then, just very briefly on the LNP as well, where are you sourcing your LNP from, and is it a novel LNP or has it been put in man before? I'm just curious if there's anything to read into as it relates to the safety of that LNP aspect of the delivery here. For the first part, I'll take the first part in terms of the starting dose, and I'll then hand over to David, who can take the second part. In terms of starting dose, we're not sharing our starting dose for some obvious reasons, but in due course, that will come out. We'll share that later following the emergence of the first clinical data. But, David, you can talk about the LNP in a bit more detail. Thank you, Adrian. We are using the latest generation lipid nanoparticle technology, with the latest generation ionizable lipid. The technology we've been using has been validated already in different contexts, and has been optimized for the very targeting that we're pursuing, i.e., the liver, with a dose range which is commensurate with the needs that we've identified and that Adrian just referred to. Yep. Just briefly to poke a little bit more on that, as it relates to the validation, I believe, has the LNP been in man, and is there clinical experience, or is it preclinical data that you're referring to there? Both, but what we're essentially relying on is recent preclinical experience. Clinical experience is ongoing as well, but it's not pursued by us. It's really essentially validated in models in primates and in other models. Got it. Thanks so much for taking the questions, and congrats on the update. Thank you. Your next question comes from Lukas Shumway from Barclays. Please go ahead. Hey, thanks for hosting the update and for taking my question. A couple from me. Have you engaged with FDA at all already to see what kind of data they are going to want to see in order to bring this into trials in the U.S.? And for.HEAL-101, have you done any fate mapping for what the truncated protein does within the cell? Because the stop codon that you are introducing is still quite a bit into the protein, so you are still going to get some translation there. Adrian, do you want to start for the U.S. deployment? Yeah, absolutely. As we said earlier, we're doing this as very much parallel activity. These are ongoing. These are all in plan. We would anticipate interactions with the regulatory authorities in the coming months. Based on our current interactions, we would anticipate to be in U.S. clinical trials by the end of 2027. Of course, that's all pending the emerging data. That is currently aligned, and there's nothing that we've seen thus far that would contradict that. But perhaps the second part would be better for David, if you think André. Yeah. Well, for the truncated protein, thank you very much for your question. For the truncated protein, as it's not detectable, by the way, we believe that the protein truncated is not secreted normally and is degraded inside the cell after translation. Most of the time, proteins that are misfolded in general go into a cycle of degradation and are eliminated quite rapidly. There's no residual protein that is a truncated protein that floats around. Maybe just an element to add. In the preclinical models, we have used humanized models with the human protein, and we actually replicated the effect that you saw where after the base editing, there was no more functional protein. Great. Thanks. Your next question comes from Salveen Richter from Goldman Sachs. Please go ahead. Hi. This is Mark on for Salveen. Thanks so much for taking our question. A couple from us. On the preclinical data you have shown, is the level of editing, I believe it was like 55% for.HEAL-101 in mice and 90% for.HEAL-201 in cell lines. Is that approximately what is needed based on competitor data for clinical efficacy in humans and what gives you confidence in the translation? Also on the catalyst path, beyond the first in human data that we could see next year in 2028, could we see any additional preclinical data, maybe in NHPs? I saw on one of the slides you showed in vivo POC data for.HEAL-101 in 2026. Just curious what that was and if you could frame expectations here. Thanks. Adrian, do you want to get started with the first part of the question? Yeah. As we stated earlier, we believe the level of editing that we are seeing in our preclinical molecules would be broadly comparable to what we have seen in other programs. Therefore, we believe that is certainly an acceptable level of editing in order to translate very positively into the first in human data. So we believe, again, based on what we have seen preclinically, that we will be at least as good as the existing therapies. On the preclinical work, the question is we are conducting a pretty sizable package of preclinical work, actually, but done with the clinical center where we are going to start the trial and with series of companies that are helping us on this will come with additional robust data and, of course, NHP data. That would be concomitant to the start of the IIT, and then potentially we will see how we communicate on the data. We are definitely doing a meaningful size of package, and IITs now require IND type or preclinical package, and we are not skipping this. Got it. Thank you. Your next question comes from Silvan Türkcan from Citizens Bank. Please go ahead. Yeah, good morning and congrats on the update. I have a question. Given AstraZeneca is also a partner and which I thought the partnership was focused very much on the CAR T side of things and also very large shareholder, can you just tell us if you have discussed these plans with AstraZeneca, what the future of this partnership looks like? Can you say anything else about these other programs you have ongoing with them? Any color on how you view that partnership evolve in the future? Thank you. Hi, Silvan. Thank you very much for the question. Well, of course, AstraZeneca has been very much involved with the discussions with this turn, and definitely the partnership will be unchanged. They are very much keen to follow up on allogeneic CAR T, and it is like piece of the agreement, by the way. As I said, there is a piece that is allogeneic CAR T cells, genetic modification for other type of cell therapies, which there is strong implication on AstraZeneca side. We would have personally also pursued on this side, but we have limited resource and had to make an arbitration. We very much strongly believe in the potential of allogeneic cells. It is essentially a question of competitive landscape that we are facing here. But the allogeneic CAR T and the next generation that we are building up with AstraZeneca is something that is absolutely exciting and mind-blowing, by the way. We are preserving all the structure inside Cellectis for the execution of this agreement. Same thing for Allogene, unchanged, and same thing for Iovance, unchanged. So really pushing forward to have all our partnership as successful as possible and keeping all the resources untouched. I don't know Arthur, if you want to add or build up on this. Thanks, Silvan. Yeah, absolutely. I think this is very critical, as you said, André, that all our partnerships are continuing in full force and effect. AstraZeneca is a strategic partner. As we had disclosed at the time, the partnerships covers oncology, immunology, and rare diseases. This is definitely a very important partner for us to be accelerating on the platform. We will keep the execution and the infrastructure around the partnership. That's absolutely critical to us. Great. Thank you. eti-cel and lasme-cel, how should we view here the probability of being able to monetize anything here compared to this being a write-off? What's just your top-level view on these programs? Thank you. Well, Silvan, we started business development initiatives since a certain period of time. We think that there's a lot of interest around these assets. The fact that the market is diminishing is just that Cellectis is not able finance it given the timelines that we have and the limited cash resources that we have. There are interests. This is a process. The business development process is ongoing, and we'll see where it gets at. It is something that we cannot continue on our side due to our cash constraints in the company. Great. Thank you. Yep. Your next question comes from Chiara Montironi from Kempen. Please go ahead. Hello, team. Thank you very much for taking my question. I am here to cover Sebastian, and congratulations on the update. I would be curious to know whether you are also looking at combination strategies for these two assets specifically, perhaps in the future or with other assets in the future. Then maybe also a follow-up on lasme-cel and eti-cel. Do you have any internal timelines in mind to monetize the program and partner it out? Thank you. Hi, Chiara. Thank you so much for the questions. Well, it is a great question, and it definitely goes to the breadth of the platform of Cellectis, and combinations is part of the strategy of Cellectis. The fact that you can combine base editors with epigenetic modifiers or, for example, transcription activators, et cetera, is a very powerful position we have currently. Considering the fact of having, for example, your question was related to the combo of an APOC3 with PCSK9. The breadth of dyslipidemia across the board is so large that there is a niche for any kind of combination in the field of dyslipidemia. Each niche is hundreds of thousands, if not millions of patients. It always makes sense, and it can be very differentiated. The idea that we have, and we will come back, updating the markets on the future development that we are doing in the field of generating new type of editors in dyslipidemia in general, because there is other potential targets, is the ability to tune up certain pathways and the biology of dyslipidemia to get the patient in a situation where the patient gets out of its disease and is, as we say, healed of his disease at the end. This is the concept we have. Yes, there is a potential for a combo between a base editor and an epigenetic modifier without increasing any risk of translocation, anything like this. It is not snapping 2x the DNA. The second idea is combining PCSK9 with APOC3 can make sense and make sense in certain type of indications with limited number of patients, but still a very large and broad population. These are the things. First, you have to test the two component independently, then the combination could start. You will see more and more this concept developing, and we believe that having all the component of gene editing platform, a very strong competitive advantage of Cellectis platform towards this approach of combo. On the second side, the likelihood of having a potential partner on our current cell therapy assets, I think, it's 50/50. It's difficult to say because you never know when you sign something up to the time you sign it. We're working hard on this, and I think that we'll probably update if there is a transaction that comes up. But we've seen in the past, before this announcement, meaningful amount of interest on these two assets. The fact that these assets give very strong data in patient, have no safety issues so far. It's like these assets essentially are in a position where they're not challenged on the medical side. On the contrary, there's a medical need, but this medical need was not the same as it was at the beginning of the year, and this might fit potentially some portfolio of certain pharma companies that we would be happy to and we're currently interacting with. But we'll update you in the meantime. I don't know, Arthur, if you want to add more because you're at the forefront of business development. Yeah. Thanks, André. As you said, we are definitely having conversation with a different breadth of pharma, ranging from large pharma that are active in CAR T to more mid-size pharma, to which this could represent bolt-on opportunities. As usual with BD, it's always very hard to give a timeline. But we will definitely pursue this conversation and strive to find the best home for these assets while we focus internally on our in vivo gene editing perspective. Clear. Thank you. Thanks. As of the moment, there are no further questions at this time. I will turn the call back over to André. Well, thank you, everyone. It was great having you all asking all these questions. We are really excited by this next chapter for Cellectis. We believe that we are finally entering what real gene editing means. It means healing people for diverse type of polymorphism, and we are really excited by this next chapter, and we will show you, I hope, that this was something that Cellectis needed to do. Thank you very much, and have a great day. Ladies and gentlemen, this concludes today's conference call. Thank you for participating. You may now disconnect.