Good morning or g ood afternoon, depending on where you are based. Thank you very much for joining the call today. We have referred you the five minutes of French quarters so that everybody can connect. My name is Hervé Affagard. I'm the CEO and co-founder of MaaT Pharma. We greatly appreciate your time in discussing our development and especially everything related to the GVHD program, MaaT013. And we're going to be presenting to you interesting data, I believe. We are a listed company, so there's a slide with the disclaimer. For your good information, you're going to have the opportunity to ask questions. So that's going to be at the end. We will answer at the end of the presentation. After the presentation from Professor Mohty, he will be the last one to speak. But you can use the chat so that we can prepare the distribution of the answers to the questions. I'm joined today by two top-notch key opinion leaders from the field of hematopoietic stem cell transplantation. I'll start with Professor Mohammad Mohty. He is the head of hematology and cell therapy at Saint-Antoine Hospital in Paris. Professor Mohty is globally recognized as a GVHD and HSCT expert. He published more than 1,000 peer-reviewed articles. So he's already one of the most prolific professors and doctors in the field. We are also joined today by Dr. Monzr Al-Malki, who is working with the City of Hope in the U.S.. He's the director of the program for blood and marrow transplant in this hospital. I'd like to underline his role in terms of pioneer because he is the first one who has treated a patient with MaaT013 in the U.S.. We are glad to have him with us today. We are honored to have them to provide a clinical perspective and share their expertise on the field of the topic of today. In terms of the agenda, I'll start with the introduction just to remind the company. We'll go with Prof. Mohamad Mohty and Dr. Monzr Al-Malki. They will present their own section. We will continue with the results from the early access program with MaaT013. We'll go to the Q&A. I'll start with a short introduction of the company. We are talking today about GVHD, which is for us as a company, the first indication for which we believe we can have a marketing authorization soon. And that's our lead program. And as you would understand, demonstrating a clinical benefit in GVHD, it's a very difficult task. And we believe that we have good data in hand. We will be publishing the results on the phase 3 in January 2025. We're going to talk today about the early access program results, 154 patients. And as I've introduced already, we're going to be also discussing the fact that we have started to treat patients in the U.S.. We are a platform company. We have different ranges of products. Some of the products are donor-derived. Today, we're going to be speaking about the donor-derived product. But we also have an exponential co-cultivation platform. We are a company very differentiated. If you look at the microbiome field, we have a platform which is using artificial intelligence to develop the drugs that we have. We have our own manufacturing facility, which is very important because the microbiome products, they are biological products, not always easy to manufacture. We have made a strategic decision to have our own facility. So I believe that's a strong differentiator. We have a safe and reliable platform to design and accelerate time-to-market for pharmaceutical innovations. In terms of the pipeline, the focus of today is GVHD, of course. Just to mention the fact that in line with the mission of the company to modulate the immune system through the modulation of the microbiome, we have several programs. We have one program with MaaT013, same candidate as the one who will be presenting today in metastatic melanoma patients, where here we want to increase the efficacy of immune checkpoint inhibitors. We have also two programs with MaaT013. The next product, which is a capsule, MaaT033. I have a presentation of MaaT033 on the next slide, but MaaT033 is a capsule. We are also evaluating and assessing the improvement in survival in any patients receiving stem cell transplantation. That's the PHEBUS trial. That's close to 400 patients that we are recruiting. That's active. We do also have a proof of concept in ALS, Lou Gehrig's in the U.S., where we want to show that the modulation of the microbiome can also help in dealing with the neuroinflammation and the management of ALS, a very difficult condition. That's about the pipeline. The product we're going to be talking about today is a pooled microbiome. The pooled microbiome product comes with certain characteristics. It is a high-richness product. High-richness has been constantly repeated into the literature as being a proxy for clinical efficacy. We have decided to go to this concept with the first product. That's why we are pooling the microbiome and to get high-richness. That's a full ecosystem. It's not like a targeted approach with one or two strains. One key characteristic of the product as well is the fact that we are producing in a consistent manner what we call the Butycore. That's the bacteria that are generating butyrate, which helps in repairing the epithelium. Our products are constant in terms of that specific attribute. The product is stored at minus 80 degrees. We have two years of shelf life for the product. On the left-hand side, you can see the difference between what it would be if MaaT013 would be a monodonor as opposed to a multi-donor pool. You can see that we have a better consistency of the product and a higher richness of the product. The product is usually administered with three doses. We have done a phase 2, HERACLES. We do evaluate the response as per what we call overall response rate, which is complete response, very good partial response, and partial response. The product has been evaluated to date in a certain number of different agencies. That's more than 10 regulatory agencies that have reviewed the product. We do have an early access program, which is pretty active. You see the demand here. We are reporting the data on 154 patients. You can see that year over year, the demand is increasing. You see the list of the countries that have authorized the use of MaaT013 as per the early access program, so it's pretty good. Not only in Europe, we also do have patients in the Middle East and North America with Canada and the U.S., and we are very happy to have treated the first patient like a little bit more than a month ago with Dr. Al-Malki in the US. We do generate revenue in France. So the EUR 2.3 million that we are reporting here, that's only evidencing the activity in France because for other countries, you cannot get paid, so that's the revenue generated from France. With this, I'd like to hand over the stage to Dr. Al-Malki, who will discuss the unmet medical need for MaaT013 in GVHD. Good morning. I'm on the West Coast in the United States, and it's still morning for us here. So nice talking to you all. Please proceed with the next slide. So as we know that allogeneic hematopoietic stem cell transplant is potentially curative therapy for a lot of malignant hematological disease. However, the main side effects that we have to work with on daily living is acute graft-versus-host disease. This is a multi-organ illness that involves skin, liver, and GI. This is when alloreactive T cells from the donor recognize a recipient antigen as a non-self and start to activate, proliferate, and expand with those clones that are going to cause inflammation in those organs. It is very common, and it is reported in almost half of the patients and happens usually within the first six months post-transplant, especially when you use a mini-transplant-like platform. It depends on the conditioning used, donor matching, graft-versus-host disease platform, and graft source. There are multiple factors that predict the incidence and the severity of this illness in this population. It is affecting almost 12,000 patients a year between the US and Europe. Mortality in those patients with the high-risk graft-versus-host disease and steroid-refractory graft-versus-host disease can exceed 50%-60% and represent a real unmet need in transplant in our field here. In this slide, we outline the current standard of care in treating acute graft-versus-host disease. This will include steroid for first-line treatment, which will fail in 50%-60% of the time based on the risk of the disease. The only drug that is available for steroid-refractory graft-versus-host disease will be Ruxolitinib, which was approved a year plus ago as a second line. Again, this has an overall response rate in the range of 50%-60%. That puts those patients with Rux-refractory patients who are going to have very poor prognosis in a range of 40%-50%. After that, we have a third line, which is actually a physician's choice type of thing. Multiple drugs have been shown in small studies or case series to have some efficacy in these scenarios. None of those are FDA-approved for that purpose. Focusing on patients that are rux-refractory patients, so those have reported data from this study published recently last year, a mortality rate of 85%, most likely due to the fact that those patients, when they get to that line, they have 80% involvement of GI. And GI is the killer in GVHD, unfortunately. And the likelihood of response is very low. And as I mentioned, those other agents have very low efficacy. And most of those patients will demise to GVHD complications. It is estimated in the range of 3,000 patients annually in both the USA and Europe to have this type of problem. And MaaT013 is uniquely positioned as the only drug of choice in the market for this type of approval. And hopefully, Dr. Mohty will show us some promising results in that regard. This slide shows the new approach targeting acute graft-versus-host disease in different lines. As you can see in the first-line setting, we have in addition to the standard of care, which is the steroids, which we have two drugs here in phase 3, Itolizumab, a humanized monoclonal anti-CD6 antibody, and alpha-1 antitrypsin. Besides that, mesenchymal cell type of approach is currently in the phase 2 earlier. Also, the second study here is showing mesenchymal cells being studied as a second-line setting. But in the third-line setting, we have the MaaT013, which is phase 3 now, besides the long-acting synthetic GLP-2 analog that is described here. Obviously, most of those agents, as we can see in the setting of cumulative use of immunosuppressive therapy, after immunosuppressive therapy, will lead ultimately and unfortunately to severe complications such as life-threatening infections, which in the majority of the time in GVHD patients is the reason for final mortality, and as you can show in these slides, the main concept here is based on this published data earlier in a good journal, shows that patients who have lower diversity, shown here in the red curve on the left side, is associated with very high risk of non-relapse mortality or GVHD-related mortality, which, as you can show on the right side, is showing a decrease or lower overall survival in those patients receiving allogeneic stem cell transplant. Thank you. Thank you very much, Monzr, for highlighting, I think, the critical issues we're facing with acute GVHD. Good morning, good afternoon, good evening, everybody, wherever you are. I hope you are keeping well and doing well. Thank you, Hervé, also for the kind introduction. So in this part, I would like to walk you through first why we are very excited about using this drug, MaaT013, in this field of severe refractory acute GVHD, and also share with you some of the data we generated based on the early access program, which was already mentioned by Hervé in his introduction and now available in many countries in Europe, in the Middle East, and now in North America. So many patients are now getting benefit of this MaaT013 product. Before sharing these data, I would like to give you a sort of vision about the mechanism of action and what's happening with MaaT013 and why we do believe it is the right choice for those patients suffering from severe acute GVHD. On the left-hand side of this slide, you can see some of the key mechanisms involved in the pathophysiology of acute GVHD. Of course, we have the allogeneic activation of donor T cells, the induction of the TH1, TH17, inflammatory response. One key element, one key factor, actually, which is the initiating process when it comes to triggering acute GVHD, is actually about the loss of microbial diversity and gut barrier integrity. This can be easily explained by the high-dose cytotoxic chemotherapy, but also radiotherapy when it is used. I think you've seen one minute ago from Dr. Al-Malki, the beautiful work published in the New England Journal of Medicine highlighting the importance of diversity, microbiota diversity in the outcome of allotransplant patients. So what's happening here is that this so-called status of dysbiosis, this is when you lose the microbial diversity, you end up triggering severe acute GVHD, but also bacterial translocation and, of course, infections. And in order to restore all this, this is where the microbiota transfer, the microbiotherapy, and the key drug is MaaT013, is going to play a role because when you have your microbial product restoring the richness, the diversity, and we are talking here about a pooled donor product, and I think Hervé in one of his slides showed you the high level of richness compared to any normal donor when you put together several donors. So really an optimal product which will lead actually to full engraftment, so restoring the diversity, secretion of anti-inflammatory metabolite, restoring the gut barrier integrity, and obviously control of inflammation through a sort of immune homeostasis. And this is critical because for the last 40 or 50 decades, we've been exclusively relying on immunosuppressive agents. And I think Dr. Al-Malki showed you one slide showing that all the current agents being explored or tested or investigated in the field are actually immunosuppressive agents. And I do believe that the success will come when you are able to restore the immune homeostasis, not by immunosuppressing the patient, which will lead to more morbidity, to mortality. And this is the reason why I think we have failed over the last 40 or 50 years in this field. And in order to support all this, I will share with you the results of the early access program. And I'm very pleased that we managed to present them continuously every year at the ASH meeting at the EBMT in Europe. And it's a very straightforward sort of a real-life program started in France, authorized by the French FDA, ANSM, and now in other countries, as you've seen from the flags on the slide of Hervé. So 154 patients were treated, which I think a huge number when it comes to this type of complications. These are steroid refractory or steroid-dependent severe acute GVHD, of course, involving the gut because the gut is a killer when it comes to GVHD. Any line of treatment was allowed, but you can appreciate that these are patients that were heavily pretreated. The median number of lines of treatment for acute GVHD was three, going from one to six. And again, Dr. Al-Malki showed you that when you reach second or third line, actually, the mortality is going to be more than 90%. So more than 90%, these patients will have really a dismal outcome. And this is where MaaT013 comes. We have a single-shot treatment, monotherapy, single agent. And you will see actually the characteristic of the patients. This is typical of what you would expect from acute GVHD, exclusively severe acute GVHD. We even had 16% of the so-called hyperacute, which is a terrible condition. And when we look to the outcome, first of all, the response rate. We know very well that the response rate is a clear predictor of survival in these patients. And when you look to the GI response rate, we do have an impressive response rate already of 51%. So more than half of the patients are going to respond at day 28, so after four weeks. But most importantly, this response is going to be sustained, so stable at day 56. And this is in sharp contrast to what we see, for instance, with a drug like ruxolitinib, where you will see a significant proportion of patients losing the response in the second months. And actually, the response in the GI is always great. Actually, when they respond, they will always respond very good, either CR or very good partial response, VGPR. So it's almost like black and white. And when you look to the overall response rate, when you look to all organs, skin, liver, GI, actually, we have roughly similar numbers. So it means maybe the product has effects that go beyond actually the GI. And that is in line with the immune homeostasis. And the result of all this is clear. When you look at one year, remember the slide from Dr. Al-Malki, the publication from Abedin and colleagues from the US, you could see a survival rate around 10% at one year. Here in those patients who responded, we do have 68%, never seen in this population. And when you consider everybody, this is 47%. And actually, if you want to have a sort of an internal control, if you look to the non-responders, this is 24%. So definitely in line with the reality on the ground. So really unprecedented results. If we dig deeper into these results, namely looking into this segment of population that we are much interested in these days, these are the ruxolitinib-refractory patients. These are the patients exactly in the third-line. This is exactly the group of patients where we treated them in this phase 3, so-called ARES trial. Hervé mentioned that we are optimistic to have the results being released next year in January. We are very eager and thrilled to see these results. We already know from the early access program, actually, that in this population, maybe the results are even better because you have almost 60% response. Again, majority of CR, 47%, 48%. It is sustained at day 56. When it comes to the survival, quite amazing, 75% at one year for the responders, 11% for the non-responders. So clearly aligned with what you would see in real life, although this is not randomized. It's an early access program, but definitely, I think we do have the positive and the negative control. And these results are quite convincing because we're talking about 154 patients. So really, the confidence interval is very tight. So very, very positive results, amazing mechanism of action. So my conclusions will not be a surprise for you, actually, because it proves clearly that MaaT013 is extremely active in those hard-to-treat patients. We do have excellent responses, including in the ruxolitinib-refractory patients. And this will translate into an improved survival thanks to this novel mechanism of action, including an excellent safety profile. I will leave you for now, and I will hand it over again to Hervé, who may wish to comment also on this slide and lead you further. We need the microphone of Hervé. I need the microphone, indeed. I was about to. I was saying thank you very much to you too. That's really a pleasure to get your insights on the field. So now, what we should expect next, the objective for the company is really to show as part of a prospective phase 3 clinical trial that we can replicate what we have seen before. So that's something we would consider as a success. And for the field, for the field of stem cell transplantation, but also for the field of microbiome, that will be a super important element. Super important element because that will be the first time we see a demonstration that a microbiome-based product will improve survival in patients. And for an emerging field, that's exactly the kind of evidence we are looking for. So the phase 3 has completed its recruitment in October. Now we are reviewing the data with the team. Christmas for us is going to be, we hope, a good Christmas with a nice gift at the bottom of the tree. We believe that early January, we will be in a position to get the top-line results of this trial, which will include the overall response rate, the characteristics of the patients so that we can compare also with what we have provided so far. That's going to be an important moment. Keep in mind also that the DSMB has reviewed half of the patients with the conclusion that what they have seen in unblinded patients was safe and higher in terms of efficacy as compared to protocol expectations. We are reasonably optimistic that we're going to have good results with the top-line results in January. Overall, the next steps for this program will be the following one. We have released the data at ASH. In January, we are going to release the top-line results. Again, on MaaT013, we are going to have the in H2 2025, we are going to have the final results from ARES with the overall survival being the last data we will be collecting. In 2025, we will start the process for registration in Europe. We have been recruiting in Europe so far with the potential in 2026, the first microbiome approved product in the field of oncology. On top of that, we're going to have also another result, which is a different result, but another proof of concept that will be important, that the PICASSO trial, which is the use of MaaT013, to show that by modulating the microbiome of the patients receiving anti-PD-1, anti-CTLA-4, you can also improve the objective response rate in patients. So that will come just after the ARES data somewhere around the end of Q1 2025. So we have been recruiting a lot of patients. As we speak today, we are treating more than 400 patients since we have started to treat patients. Now we are at a stage where we are accumulating the data, and we will continue to communicate those data to you. So that's in a nutshell, the next steps. And with that, I've seen there's already many questions. So I'll take them in order. My team is ready also to respond to the questions. You'll see Dr. Gianluca Giaccone, our CMO, joining in a minute into the panel. We do also have the rest of the team, including the CFO and the rest of the team. They are connected. They are in the room with me. If they need to show up, they will show up. Do not hesitate with your questions. The first question, let me take the question, is from Jacob. Thank you, Jacob, for your questions. Can you provide guidance on when you expect to start a phase 3 trial of MaaT013 in GVHD in the U.S.? That's dependent on financing that we will be in a position to start the clinical trial in the US. Today, for us, it's too much of a risk to embark into the clinical trial without more financing. Just remind the situation, we have an IND open for the ARES U.S. part of the trial that has been cleared, authorized by the FDA early 2023, so that's where we are today. We are still here, and once we have the financing, we will, of course, rediscuss again with the physicians to make sure that we are all set and we will initiate the clinical trial, so the products are ready. They are FDA compliant, and that's really a question of financing. The second question is from Benoit. Do you plan to distribute MaaT013 out of Europe and the USA? Today, as you have seen, we have started to treat patients in the Middle East, so I think we have proven today that we can deliver patients, we can deliver products for patients where it is needed, so we do not have logistic constraints. We do stick to our mission to help patients. So if there's a patient in China, in India, there's nothing preventing us from serving the patient. It's fair to say that because of the data that we have generated, we receive more and more requests from everywhere in the world. So we have the supply chain in place to deliver like everywhere in the world. So it should not be a problem. The third question is from Jacob again. We see that the response rate in the early access program improved compared to the phase 2. Can you provide some insight into this observation? And do you expect third-line patients to respond better to treatment compared to second-line patients? So is Gianluca Giaccone connected? I think we have a technical problem, of course. So Aline, you're connected. Did you hear the question, Gianluca Giaccone? I did hear the question. Thank you for bringing it to me. And really, it is true that we observed some better results. But I think several factors can really contribute to this observed difference when you compare the phase 2 HERACLES data and the EAP. So I'd like to, first of all, point out that the HERACLES study was exclusively including high-risk subjects with grade 3 and grade 4 acute graft-versus-host disease. And they were also exhibiting refractoriness to high-dose corticosteroids. And when you compare these criteria to the EAP, you observe that the EAP is actually also open to patients that have clinically milder acute graft-versus-host disease or that have also corticosteroid dependence. And so basically, this means that they are not really refractory to corticosteroids, but they require ongoing corticosteroids for GVHD control. Actually, the population looks a little bit milder in terms of expected responses to treatment as compared to the original phase two study. I would also add, of course, that the response rates that we have seen with HERACLES should also be interpreted with a little bit of caution. That's because, of course, the conclusions that can be drawn from this data are, of course, limited by the sample size of that study. Now we have a much wider cohort in the EAP. Perhaps I may also potentially hypothesize that there have been advancements in patient management. Now our understanding of the clinical context where MaaT Pharma enema can actually drive results is improving. Of course, this could also support these enhanced overall outcomes in the EAP. Can I, Hervé, add a couple of things to what Gianluca has nicely said? From a clinical standpoint for us in the clinic, and although we may view the steroid dependence as a less severe situation, but actually, this is a terrible situation for the patient because obviously, it exposed them to the continuous use of steroids and all the deleterious side effects, morbidity, and even mortality. So from a clinical standpoint, this is also an unmet need. The other remark I would like to add is about the second part of the question, which is, do you expect third-line patients to respond better to treatment compared to second-line? My short personal feeling and my short answer is probably yes. And this is very surprising to anybody saying, oh, the third-line will do better than the second-line. But I think Dr. Gianluca Giaccone highlighted that there has been progress in the management. And the key progress, and Monzr, I think, alluded to this, was the approval of ruxolitinib. So these patients are receiving ruxolitinib. And I'm convinced, based on the mechanism of action, based on the immunology, that there is an amazing synergy that can exist between using a JAK inhibitor and restoring the microbiota. So yes, I do trust completely these results of the early access, even in the third-line, which they look like magic, but they are true. And we treated patients there. So I've seen these patients. And as we are in the clinical section, I will regroup certain questions. Maybe the first one is for Monzr because recently, you have made the decision to use MaaT013. So the question is, what are the values of GI overall response rate for the KOL? What are the values of GI ORR at day 28 and one-year OS that you would consider clinically relevant? Exactly. Thank you so much for the question. It's important to understand in GVHD, the fatality comes all from GI. I have been taking care of a lot of patients during the last 15 years and have never seen a GVHD of the skin or liver that could cause a mortality for a patient, or maybe few cases over the long years. But I think the GVHD is the reason for patient mortality. It is the reason for being in the hospital for long. It is a reason to have more infections due to breakage of the GI barrier and leakage of all those bacteria in. It is the reason for a lot of treatments not being absorbed and not being effective. So there's a multitude to this problem. I think the GI GVHD management is the way to go for this type of population. I think something that is directive to address the GI deficit and the problem where will be probably very important to address this kind of issue. Patients who had, I mean, I just want to comment on what Dr. Mohty mentioned about that combination. Actually, this is a very promising combination that I think also I agree with Dr. Mohty that the synergistic effect of JAK or ruxolitinib, I'm sorry, with MaaT013 will be a very important next step in investigation. We will not know until we have the study. I think the first step is to get it approved for third-line and then compete on the second-line setting. Based on what we just said, Dr. Al-Malki, can you also share your experience as you have treated your first patients recently? Yeah, this is a very nice young lady, 38 years old. She had really bad leukemia and had relapsed with minimum residual disease at day 100. That triggered us to start her on hypomethylating agent like treatment for post-transplant relapse and withdraw immunosuppressive therapy. That is the first step that you would do for post-transplant relapse. At that time, a patient triggered bad GVHD with more than 3 liters of bowel movements a day, which characterized her or graded her as a grade 4 GVHD and was mostly GI. And the patient went through multiple lines of therapy, high-dose steroids, followed by different clinical trials. And then JAK was added and then ultimately used multiple immunosuppressive therapy in a third-line setting, including basiliximab, infliximab. The patient at best had a very transient response to one of the agents, but continued to progress. And at that time, we contacted you guys, and you guys helped a lot with setting up this type of treatment, which I thought was promising and explained to the patient. The patient was very excited on signing up for this. And after regulatory approval, the patient received treatment almost a year and a half ago now, sorry, a month and a half ago now. And I think now she's on day 28; she achieved very good partial response. The patient got discharged from the hospital a week after treatment, after being in the hospital for three months. And now she's coming to clinic. And towards maybe a week after day 28 or 10 days, she went and achieved CR now. And she is following up once a week in the clinic, doing great. This is the miracle, Monzr. You made my day. This reminds me of our first patient. They were dying, and they were resuscitated. Amazing. Yeah, no, I think good work and shown the data that you presented. Then later on, once we have the results of the phase three, I think all this will advise us on how promising this approach is. Yeah, thank you very much. That's really in line with the mission of the company, indeed. There's a question maybe in terms of the methodology, maybe for Dr. Gianluca Giaccone. Can you remind us why the development in third-line is single-arm as opposed to randomized? Sure. So we have, in the course of this presentation, described what the outcome is in patients who have, I mean, who have a corticosteroid ruxolitinib refractory acute graft-versus-host disease. These are patients whose median survival is approximately one month, and the long-term survival is of the order of 10%-15%. So, of course, in the context of this slim prognosis, designing a randomized study wouldn't simply be ethical because you would have an arm of patients that would almost invariably face a short-term demise and then patients that would respond to this treatment and have long-term survival. That's basically the reason. And of course, the conduct of a single-arm study has to be seen in that perspective. We'll regroup with certain questions because we are already at more than 25 questions. So I'm trying to regroup now. Can you also, Dr. Gianluca Giaccone, share with the group what we could consider after GVHD? What those data will, in which way it will inform us on the next step and what kind of indications we might be targeting? Sure. So with respect specifically to MaaT013, I believe the important homeostatic effect of the immune system may lead us to explore the fields of, of course, modulation of immunotherapy strategies that we already have. Certainly, this is valid in the context of immune checkpoint inhibition for solid tumors where we do observe a high incidence of primary refractoriness. But of course, the story doesn't end here. I would say that future potential endeavors may be involving immune therapies that we are using in the context of several conditions in cancer, including hematology. I would also probably say that the entire inflammatory power of MaaT013 in the context of a very severe status of hyperinflammation, that is, of course, acute graft-versus-host disease, might give us a very strong proof of concept to also inflammatory conditions that we face in hematology. So I believe that the floor is really open after these results to really go in many different directions. Thank you. And I have again two questions that would serve as a bridge to the more corporate development questions. The first one is regarding the evaluation of ruxolitinib. Do you think that response to ruxo at day 28 is reasonable in patients with high-risk acute GVHD? I don't know. Mohammad, maybe you can take this one. The question is about whether we consider the response rate as being reasonable. Well, I don't think I need to comment on the response to ruxo because at the end of the day, the response, we may consider it as modest or not, but still, it was approved for steroid-refractory acute GVHD. And actually, it was around 60%. So 40% actually are not responding to ruxolitinib. We should be aware of this. And then by day 56, the 60% response of ruxo is declining, and you're losing around 20%-25%. What I would like to emphasize, and this is really where the story becomes very exciting, is that when you look to our response rate in the early access program in the population which is ruxo refractory, so if you follow the logic, you would expect a lower response rate compared to what ruxo achieved in earlier line. Actually, we have even a slightly better response rate. I would consider that the response to MaaT013 is not only reasonable; it's even beyond expectations. We've seen the results. What is really interesting about acute GVHD is that there is a direct correlation between response and survival. When you respond, when the patient responds, they will live longer. I think there was also, I've seen a question about declining survival. Actually, I don't believe there is a declining survival over time, but please remember, these are patients who are treated for leukemias and other malignancies. So they may die from the relapse of their malignant disease, which is a totally different story because overall survival is not exclusively related to acute GVHD. So I thought that this needed to be highlighted because I think a member of the audience asked this question. Yes, indeed. So there are a few questions also on the early introduction of MaaT013, meaning before ruxo refractoriness, and there are figures that have been put, introduction of MaaT013 after 14 days and everything. And I think it comes together with what we have said earlier. Third-line is really the we need a label. We need a proper design clinical trial. We need to penetrate the market with a very clear population. And then, of course, we see because of the profile of the product, which is really low toxicity, if no toxicity at all, we could also evolve in other lines. We do report on the early access program, already 7% of the patients being second-line patients. So in combination with ruxolitinib, we do see a potential as well. Going more on the partnership side of things, because of the fact that we have very strong data on this setting, and we see there's adoption also in other indications and in other lines of treatment in GVHD, we see also an increasing interest from pharmaceutical companies. There's also a question, which is, how do you see the microbiome evolving within the next two to three years? The reason why I'm talking about the combination with existing drugs, for me and for the company at the strategic level, we really do see the microbiome more and more being in a position to treat certain diseases as it is for GVHD, as it is for Clostridium difficile. Also, we see more and more microbiome has been used as another pillar with any kind of anti-cancer treatment, but any kind of immunosuppressant or also in IBD and others. So we really do see the microbiome going into that direction. We see more and more companies generating data in non-Clostridium difficile indications. Just in Europe, we have three companies, one developing in NEC, the other one in IBD, and the other one, MaaT Pharma, in GVHD. So we see more and more opening. What we need now is to establish strong partnerships with established pharmaceutical companies so that the industry will develop itself. That's exactly the way we see it, and that's the way we see the field evolving within the next two to three years, I would say. So I'm looking at the questions again because I'm sorry, but there's too many questions. On your slide, the survival of responders declined over time. Is there any method on how you could measure the microbiome content over time and administer a further dose if required to restore the optimal level? Maybe Dr. Gianluca Giaccone, you can take this one. Sure. Of course, we do have thought about that, and we do allow the possibility of a fourth dose in case clinical response is less good than what we expect or if there is any indication that the graft-versus-host disease might be coming back, so I think it's interesting to note that the administration of fourth dose might potentially be able to revert the acute graft-versus-host disease flare, so this means that the possibility of reverting graft-versus-host is not jeopardized by the fact that the patient has received previous MaaT013 doses. I think this is an important aspect. Of course, just to answer the other part of the question, there are ongoing studies, and there will be studies in the future that will allow us to establish a correlation between the clinical outcomes, meaning both the response rate and the maintenance of this response over time and the characteristics of the microbiome. Of course, it's important to note that these are studies that are basically correlating the metagenomic data with clinical data. And so, of course, patients are needed, numbers are needed in order to make robust correlations, but certainly, we're working on that. So if you allow me just to add two quick notes to this. Unfortunately, in the Early Access Program, we didn't check for the sustained engraftment or not, but we know from the HERACLES trial and other experiments that once a microbiota is in, it is very solid. So this is clearly very good news. And the other news is that although we're not giving maintenance treatment with MaaT013 today, but we know that in the ARES trial, according to the physician decision, some patients could benefit from an additional enema. And we know it is feasible, it is safe, it is useful. So clearly, the answer is positive there. Yeah. And maybe a last question for Dr. Monzr Al-Malki. Why do you think there are two questions for you? What's the perception from physicians in the U.S. regarding MaaT013? And the second question is, why do you think there's so little competition in the third-line setting? So for the first question, I think, as we mentioned during the session, there is multiple data coming out now and educating us about different types of aspects of the microbiome, which bacteria might be beneficial, which one is not, and how we could improve this and how we can use it. Obviously, the main issue with this type of management has been in the past, the delivery method. And now that we are seeing that this study is showing viability for this type of delivery, I think it will make it easier for people to adapt. I think the future will be great. The plan to have a study open in the United States will make it easier for people to adopt that type of administration method. There is another company where they are delivering also capsules that could be another way to do it. But I would wonder the difference between the response rate in both where you have a method where you deliver directly to the organ involved versus when you have to go through multiple processes to get the product to where it belongs. So I think the study will help tremendously to improve people's adaptation to this type of approach. But I think the unmet need has been shown here, and it is significant. And with those good data that we have and Dr. Mohty presented and you guys all discussed, I think there is a big, big need for something that is effective like this. And then the second question, sorry, how? What's the perception from the physicians on the company? Yeah. I think you have answered it. Yeah. Okay. So we are at time. I want to thank the speakers today. Thank you very much for your explanation. That was really, really super interesting. Thank you to the participants on the web. We will continue to keep you posted. Next step will be early January, we hope. So thank you very much, and enjoy the parties for Christmas and New Year's Eve, and take care of your families and friends. Thank you very much. Bye-bye. Thank you. Thank you.