our CFO. Good morning, everyone, and welcome to our 3rd quarter business updates and financial results. I'm Namir Hassan, CEO of Zelluna, and I'm delighted to be joined by Geir Christian Melen, I can have the next slide, please. And the next. So today we will be covering our key events for our 3rd quarter. We'll revisit briefly the TCR NK technology. We'll go into more detail on our lead ZiMA-101 first-in-human clinical study, and then we will cover a financial update and finally finish with a summary and outlook. So I can have the next slide, please, and the next one. Thank you. It's really been another defining quarter for Zelluna with tremendous progress across all areas of development. I'll focus here on our lead clinical program. And perhaps most importantly, we have really seen tremendous progress in the recruitment and dosing of patients which are on track. This is and can tend to be a challenge for early phase clinical studies, and I'm delighted to say that we have treated 2 of 3 patients at dose level 1, and we expect to complete the cohort and treat the 3rd patient in Q4. The Clinical and biological assessments, so that includes tumor imaging assessments and patient sample analysis, remains ongoing for the patients. This has been really underpinned by the strong progress and the strong engagement that we have seen from our clinical sites and our clinicians. In fact, the sites overall have prescreened over 30 patients across different indications for the 2 biomarkers that are necessary, MAJ-A4 and HLA-A2. And because of this high volume of engagement, we're able to guide today that we expect to treat and fill cohort 2, the second dose level, by early Q2 2027. This really has been a tremendous start for the clinical study. Now, second to that, we have also seen encouraging initial clinical observations. No dose-limiting toxicities. The safety profile has been favorable. This is a very important point when it comes to cell therapies where we can see and have seen toxicities in patients with other types of cell therapy modalities. We're also looking at samples from patients. As you know, these samples include blood samples. They also include biopsy samples. And what we have seen so far are the distribution of cells in the system, systemically in the bloodstream, is as expected. And we have also picked up some immune marker changes. And so what we're looking for here are biological traces for the effects of TCRNK, for the effects of our therapy. And we're picking up some changes that suggest we are seeing some immunological changes as a consequence of treating with TCRNK. These changes have also been seen with other types of immunotherapies. And so we continue to assess what these changes mean and how they may potentially be linked with the effect of the treatment. Parallel to that, it's also a delight to mention that our manufacturing transition is on track. We have a new CDMO that we have been working with, and the first run has been completed with product characterization ongoing. This is a very important element of any cell therapy where manufacturing needs to be adaptable and versatile. And potentially transferable between manufacturing sites. And so what this run has demonstrated and highlighted is the potential adaptability of the manufacturing platform that the team have been developing over the last years. And we announced last night that we were delighted to receive an award from the Norwegian Research Council of around 16 million NOK to advance our manufacturing program. Lastly, and also very importantly, we're seeing growing clinical evidence in the field for the TCR NK concept. This is some data that has emerged from the MD Anderson where they have a TCR NK therapy. It targets a different target, NY-ESO. are able to deliver move on to the next slide and just revisit briefly why our platform technology is exciting and differentiated. We have a differentiated platform whereby we have T-cell, TCR NK cells. It's— and we also have a clinical stage programme which we're very excited about. And we have been updating on. We now have seen external clinical evidence demonstrating that the concept can work. It's in a different setting, in this case multiple myeloma, but what they have shown is a complete response that is durable with this type of therapy. in a multiple myeloma patient that has been heavily pretreated with multiple lines of therapy, including highly innovative CAR-T therapy. Prior cell therapies. This is a very important point and goes to reinforce the concept and the approach that we have, which is that TCR NKs in concept CRNK. If I can have the next slide, please. So just a couple of slides to briefly revisit the context. Context is important. We're operating in a cell therapy space. And these 2 slides demonstrate 2 axes of what it means to operate in a cell therapy space. The first is to demonstrate that small patient datasets within this space can really command high value when it comes to approvals. Here shown are multiple approvals with the number of patients that have driven these approvals. Showing that approvals for cell therapies can And really drive durable external clinical evidence demonstrating that the concept can work and really drive durable responses. We also have a scalable manufacturing platform with layers of IP, including a concept patent. So this is a patent protecting And for that is that in general, cell therapies, when they work, they work of what happens when you then increase the number of patients. In fact, just a week ago, another company with a cell therapy, Iovance, that have an approval, have treated another indication. what one can expect later on. If I can have the next slide, please. Another access to consider when it comes to cell therapies is the potential value of small patient datasets where we have seen multiple transactions. types of transactions is that it is symbolic also of the shift we have seen in cell therapies and the appetite for Separate to the approved indication, they treated 8 patients with synovial sarcoma and had seen 4 responses in those patients and have immediately moved to a registration study on the back of the 50% response rate on relatively few patients. So small patient datasets can be predictive of over the last couple of years that have involved small patient data that have driven acquisitions and partnerships. And important to remember with these off-the-shelf scalable cell therapies. And that's exactly the arena that we are in. We are offering an off-the-shelf scalable cell therapy platform. In our case, to treat solid tumors, which is where the largest cancer burden is and the greatest commercial possibility. If I can have the next slide, please. company over Q3. We have had a great start when it comes to site engagement and patient identification. This can be a big challenge for early-phase clinical studies, and I think a testament to the excitement around the program and the platform. We're seeing huge engagement from sites and, and the clinicians, and now we're building that momentum where we're able to guide on when we expect to complete the next dose level, dose level 2. And incidentally, dose level 2 is 3 times higher dose than dose level 1. So it's a significant uplift from where we are today. So what have we done over the last quarter and what can we look to the horizon towards? We have really transitioned to become a clinical stage Also continue to build on the platform and the pipeline with manufacturing and working with our new CDMO, and also our pipeline where the lead pipeline program is another target, KKLC1. that is expressed across complementary cancers to MAJ-A4. and build the data on the potential of the TCR NK platform. And that, we believe, will really open strategic options for the organisation moving forward. So we're moving and building our clinical data with a focus on clinical execution in order to really develop the understanding If I can have the next slide, please. So just to revisit the TCR technology and pipeline, we have typically done this in our updates. We can keep this relatively brief. 4 pillars, if you like, of the company and the platform technology. We believe it's a game-changing platform with a de-risked concept and path. We'll come back to that a little later. We have a protection on the concept, the TCR NK concept, which we think really holds tremendous value if we come to show that the platform is able to deliver responses in patients. We have, we believe, near-term value inflections. We're moving and advancing through with momentum through our dose escalation study. We expect to fill Cohort 1 in Q4, and we are able to guide on filling Cohort 2 by early Q2, which will all be very exciting to build that clinical data, tumour imaging, sample analysis, and really build a comprehensive picture of how the treatment is working in patients. And all of this operating within the arena of cell therapies where we have seen the value, high value of small clinical datasets. If I can have the next slide, please. And so we talk about the de-risked concept. We now have updated on the external data that has demonstrated for the first time a TCRNK delivering deep responses in a late-stage multiple myeloma patient. We also believe the components of TCRNK are de-risked. The T-cell receptor itself is a validated scaffold, targeting scaffold. We have 2 approvals that are driven by T-cell receptors in solid tumours and NK cells themselves. Are, we believe, a validated cell type with decades of clinical data demonstrating the safe use of the cells and also potency. In liquid cancers. And so we bring those 2 things together in one cell to really drive responses in solid tumours. And that way, we believe we're addressing the main challenges that are marking the difficulty for current cell therapies to really drive scalable treatment for solid tumours. And so moving on to the next slide. These are the challenges that I had touched on. 3 main challenges. The first is the effectiveness of cell therapies in solid tumours, where most therapies go after a single target. And what that means is that the cancers can avoid that target whilst perhaps showing a response initially. So patients tend to relapse with those types of therapies. With our TCR-NK approach, we have multiple ways of recognising cancer. We've demonstrated that in our science that the talented team have been able to produce and publish. And so with recognising cancer in multiple ways, we aim to reduce the prospect of cancer escape. The second challenge has been scale and cost. All the therapies that have been approved for cell therapy are ones that are specific to each patient. So every patient will get their own manufacturing batch. That comes with cost, that comes with complexity, failed manufacturing runs, and ultimately difficult and challenging to scale. Whereas we produce an upfront batch, frozen, hundreds of vials in the freezer, accessible and immediately able to use those for patients. So it's a scalable, lower-cost solution. And finally, the safety challenges that many cell therapies face, including some of the latest innovative therapies that we have seen, such as in vivo CAR-T, where we have seen toxicities emerge in those novel platforms too. So far, we have seen a favourable safety profile with our TCR NK platform. We know NK cells generally are safe. They have lower risk of toxicities that are typically seen with other cell therapies. So we believe collectively, the TCR NK approach can provide effective solutions to all 3 challenges. And so moving on to the next slide. Our manufacturing platform that we're now working with a new CDMO on is one where we're able to upfront generate hundreds of vials that are destined to treat many patients, and those are frozen down and can be used immediately when needed. And so this scalability prospect for our platform really addresses a huge challenge in trying to meet the massive unmet need which is the solid cancer space. And so moving on to the next slide. I'll spend a little time on our first-in-human study. As you know, we have 2 sites that have been activated that are up and running and that are recruiting patients. Highly engaged sites where we have built strong momentum. Professor Fiona Thistlethwaite from The Christie is our chief investigator. This is a quote that she has in taking them through the prescreening. the— in her reflections on the start of the trial. Again, encouraging progress to see the recruitment, identifying high volume of patients, So that is the first eligibility test looking for MAJ-A4 and HLA-A2. And we also have Andrew Furness from the Royal Marsden in London, also identifying patients and channeling those patients into the study. So this is crucial and fundamental to any early phase clinical study is to really build momentum in patient recruitment, particularly for those early doses. So one can get through the first dose levels and move to the higher dose levels. So very pleased by this engagement and progress. Moving on to the next slide, please. And so an illustration and a reminder of the format of the study is a phase 1 dose escalation, 3 patients per cohort, 3 dose levels. defined, and we have a 4th dose level that is flexible, not predefined. We have 4 indications: lung, ovarian, sarcoma, head and neck cancer. And patients have been identified and have been screened for the biomarkers MAJ-A4 and HLA-A2 across all 4 indications. We are treating patients that are heavily pretreated. These are very sick patients, heavily pretreated, sometimes with high disease burden with no other options, unfortunately for them. And so these— that's the state of patients that we're treating. And so we're really trying to the continuation of the study on account of the favorable safety profile. You can see there in the illustration the process that a patient will go through, lymphodepletion, develop and induce responses in quite a poorly patient population. We have oversight by an independent safety monitoring committee. And we had announced in August that they had reviewed the first patient data, the sentinel patient, and had licensed and recommended to prepare the patient for the cells, 3 infusions of the cells, safety observation period, and for the first patient, at least in the cohort, a review of that patient's data. To allow the next 2 patients. And for each cohort, by the end of the cohort, we also have a safety review by the independent committee for the entire cohort. We really comprehensively analyse the patients across various axes. So we look at tumour responses by imaging, tumour biology, cell kinetics, immune biology. And I'd commented earlier on some of the findings we have seen for those in this early phase analysis. And so moving on to the next slide, safety is a really important feature when it comes to cell therapies and is really growing to become a differentiating feature. For cell therapies. Safety can limit the potential scale and use of cell therapies where safety can be a challenge and problematic. Those therapies would need to be used in specialist centres. And so limits the scale to use the therapies in more community hospitals. And we have seen toxicities with CAR-Ts. And also with the emerging in vivo CAR-T platforms with neurotoxicity, we've seen cytokine release syndrome. And also some graft versus host disease. And so there are a range of toxicities that we may see with some cell therapies. feature potentially for the platform. That so far for TCRNKs, we haven't seen so far a favorable safety profile. And so this really is growing to be a differentiating And so moving on to the next slide. This is to demonstrate what areas we're looking at and what are we looking for essentially in the first patients treated. Principally is to demonstrate safety. This is a phase 1 study, and that is always the principal driver. It's a first-in-class MAJE-A4 targeting T-cell receptor NK. So even more important to demonstrate safety. And so far in the patients that we have treated, we have had a favorable safety profile with no dose-limiting toxicity. TCRNK in the blood. And so with some changes that are seen, we're really assessing what those changes potentially might mean with respect to TCRNK effect. And ultimately, of course, we would be wanting to understand the effects on the tumour and really want to observe tumour shrinkages through imaging. And so that those assessments continue, and we expect a greater opportunity to observe those effects as we move through the dose levels, where dose level 2, for example, gives 3 times the exposure of cells compared to dose level 1. And so with our guidance on when we expect to treat patients in dose level 2, we're really excited to look forward to getting there and continue to assess the effects on the tumour now. And as we continue to move through the dose levels. So that's very important. Next, the next layer is to demonstrate proof of mechanism to also inform the potential of the platform. And for that, we're looking at sample analysis, tumours, blood samples. This is ongoing, and we have seen some encouraging changes in patients with peripheral immune marker changes. As mentioned, we're looking for essentially traces and biological effects of review the entirety of the data for the patient and recommend the recruitment of the next 2 patients. And that was in August. Second patient was dosed in October. And throughout that period, we've been building momentum with identifying patients across the indications and smoothing the infrastructure to the testing needed for the 2 biomarkers, HLA-A2 and MAJE-A4. And now we're in full swing with that momentum built. Over 30 patients that have been tested for the 2 biomarkers. And we expect to complete dose level 1 in Q4. And we can guide now on when we expect to complete dose level 2 by early Q2 2027. All of that is a credit to the team at Zelluna and a credit to the teams at the 2 clinical sites. They've really shown a very strong engagement with the study. So moving on to the next slide, just to take you through the sequence of events that we have had over the last quarter or so. We've had 2 patients treated. The first patient was dosed in July. We then had a 1-month safety period, and after that, we had the independent review committee And so moving on to the next slide, just to take a moment because this is very important. The external growing evidence on the potential of TCRNK, perhaps now underpinned by the first clinical data with a TCRNK program from the MD Anderson. Where they had announced a complete durable response in a multiple myeloma patient. So what was reported? It's a response in a heavily pretreated patient, a patient that has been treated in prior lines of therapy with a cell therapy, including BCMA CAR-Ts, which can be very effective, but they relapsed with that. And they went on to get the TCRNK and had a response with TCRNK that was complete. You can see there in the stains in the picture on the right, staining for the cancer cells and the target Nyezo, where there's complete clearance in the bone marrow of those cancer cells. durable deep responses, in this case in a myeloma patient. And what we're aiming to do in our study is to demonstrate responses in solid cancer patients. So the TCRNK can target, kill, and drive responses in late-stage cancer patients. Now, this is important because it demonstrates that the concept, the approach, the TCRNK engine, if you like, is able to really drive I can have the next slide, please. And so looking to our pipeline, we have a pipeline beyond MAJE-A4 that is made up of KKL-C1, which is the next in line. And then behind that, PRAME. It's a pipeline which has broad tumor potential, multiple cancer indications, as you can see, really large cancer types with high unmet medical needs. And as we have been building our platform, truly a platform, we also leverage on the platform knowledge and infrastructure So pipeline programs can plug into the manufacturing platform. For example, they can plug into the part, the regulatory Pipeline programs can plug into the manufacturing platform. For example, they can plug into the part, the regulatory So pipeline programs can plug into the manufacturing platform. For example, they can plug into the part, the regulatory in grants from the Research Council of Norway to support our clinical study. a loan or a commitment under a licensing agreement. And we also raised funds in June, gross proceeds of $58.2 million. And we're very pleased that we could announce earlier this year that we received $60 million NOC And as you might have seen yesterday, we announced that we have received another grant from the Research Council. It's almost $16 million as well. in support to further advance our TCR NK manufacturing. Then I would like to move on to the profit and loss and the cash position on this slide, where you can see the quarter this year compared to the quarter last year and year-to-date figures. I will not go into any details, but just mention that our payroll and payroll-related expenses is substantially lower than last year as we have reduced our headcount. substantially. The R&D costs are about 14 million, or less than 14 million this quarter, and the key contributor to the cost here is the startup of the clinical trial. It's quite a heavy cost to get that trial up and running. And we have, as indicated, enrolled the first patients this quarter. Order operating expenses. Sorry, if you go about one slide back. Order operating expenses, whereas influenced this quarter by a few events in terms of the private placement and share issue and general meeting. But then compared to the 3rd quarter last year, we have substantially lower cost year to date this year because we don't have any business combination-related cost anymore. Then I'm happy to take you to the next slide. Where you see the quarters through it from first quarter last year to this quarter, and you can see how the figures compare over time. I will not go into the details here other than saying you can see the number of employees demonstrating the substantial reduction in the headcount that we have gone through post the business combination. And next slide, please. And here you see the quarterly operating cash flow, which were substantially higher last year and now is more stable around €20 million. €20 million plus per quarter. And if you look at— when we look at Q3 especially, the operating cash flow is in line with the operating profit adjusted for depreciation and other non-cash items. The cash position was reduced from €86 million at the end of the second quarter to €60 million this quarter. Importantly, though, is to mention that we have not received our tax refunds, skattefond, tax credit for 2025 yet at the end of Q3, which we then expect to receive this quarter. Q4, and we also not received any payments yet under the €60 million grant for the clinical trial. We expect that to happen shortly, and most of that will then come in Q4 and in 2027. Then I think that completes my review. On the next slide, I would like to hand it over to you, Namir, for a summary and outlook. Thank you, Geir. So if I can have the next slide, please. I'd like to finish by bringing together why we believe this is a really exciting phase for Zelluna. So starting on the left, what we have achieved and what we have de-risked is that we have really gone through our preclinical work, and demonstrated the potential preclinically. We have generated a GMP batch of material that's frozen and now being used to treat patients. And we have world-class clinical sites active and dosing patients and really strongly engaged in the program, which is exactly where a development program would want to be at this early stage. All of that with a protected TCR-NK platform. And so Then looking below, the external evidence that continues to grow on the potential and the confidence in TCR-NK. We have the TCR data that we know demonstrates the validity of the T-cell receptor as a targeting platform, the natural killer cells and the data on natural killer cells demonstrating their safety and potential activity. And now with growing evidence for an independent TCR-NK demonstrating that the concept can drive responses in late-stage cancer patients. So then if we move our focus to the central bucket, patient data, which is our highest priority now, moving through dose escalation, treating patients. The initial data is emerging and encouraging, and we're now able to look towards when we may be able to complete higher doses with guidance on when we would fill Cohort 2 by early Q2 2027. And why does it matter? That's shown on the right-hand bucket. It matters because small patient datasets where we're able to demonstrate the biological translation into patients can really drive high value, high value in terms of transactions and high value in terms of the patients needed to then drive approvals. The predictability of those small patient datasets is very clear when it comes to cell therapies. So we're very excited. We're very excited by the progress. We're very excited by the potential to continue to build on the clinical data and hopefully demonstrate the potential of the platform to drive value and create value for patients that are really in dire need of new therapies, and then of course, in parallel, value for shareholders. Thank you very much for your time this morning, and I'll be delighted to take any questions. as they come in. Thank you, Namir. This time, we have received quite a few questions. So let's see if we can deal with all of those. They are related to the clinical trial and our clinical programme. So the 2 first questions are related to why— if you could explain why no tumour response or imaging data have been disclosed from dose level 1 so far. And what criteria will determine when you're ready to report clinical efficacy data? And kind of a related question is, is the decision not to disclose clinical efficacy data driven primarily by the small patient number, short follow-up, the low initial dose level, or absence of sufficiently mature data? Very good questions, and thank you for those questions. And of course, this is an attention point for us, of course, as well. Now, the phase that we're in is early. We've treated a couple of patients. And so the primary drive for this phase is to establish safety. Now, We are clearly assessing patients for the potential for any responses in tumour as we are assessing patient samples. But at this early stage, with only 2 patients treated, it's premature to speculate or comment on any of that data. And where we would establish and communicate the data, we would need to be confident in any communication that we make. But of course, we're very mindful of that. And we'll be very diligent to our obligations, and we would communicate when the time is right, when we have sufficient, when we believe we have sufficient data to make a communication and a meaningful comment on imaging in particular. So to the second question, and I think the layers of explanation in that second question, in terms of us being early phase, in terms of us having short follow-up so far, I think all of those are true. And I would resonate with those explanations. So I would say as we move forward, we'll continue to build on the data. We've treated 2 patients. We're waiting on imaging data. We have a 3rd patient that is scheduled to be treated, and of course we'll need to receive the imaging data from that patient. And so as we collect all of that data, we are, of course, mindful about potentially communicating to the market when we believe there is meaningful data to communicate. Thanks. And then we have a couple of questions related to what we have seen so far. You have touched upon this, and you have elaborated somewhat on it. No, but just maybe it's good to repeat, and maybe you can say something more along the lines of, well, around cell kinetics are in line with expectations. Could you explain in simple terms what this means and what you have seen so far in patients? And then the other question is, you also mentioned changes in pro-inflammatory immune markers after treatment. Is this an early indication that the CIMA MH-401 cells are doing what you hoped they would do in the body? Very good questions. And so with the cell kinetics, in simple terms, what we have seen is when we look for the cells in the bloodstream, we can see that they pretty rapidly disappear from the bloodstream, and we assume they're moving into the tissues. And this is a phenomenon that has been seen with other NK therapies where you infuse the therapy, and within a day or so, they disappear into the tissues. And so we have seen similar kinetics with our TCR NKs. Our assumption is that they're moving towards the tumour. And we're looking at that, of course, and that assessment is ongoing when it comes to biopsies, for example. And then when it comes to the immune marker changes that we have seen, of course, What we're looking for are biological traces of the effect of TCR NK. But we're looking for those traces in the bloodstream. Of course, the actual effect of our therapy will be on tumours, but you can sometimes pick up traces in the bloodstream that would indicate the cells are acting in the tumour. So this is quite a broad analysis where we're looking at the whole field of immune markers, and we have picked up some changes that occur once we infuse the cells. And these cell— these changes are what are called pro-inflammatory changes. In essence, the immune system seems to be kicked— kicking off. And we have seen similar changes with other immunotherapies, whether that's cell therapies or bispecifics. We don't know exactly what it means yet, whether it means that we're seeing the TCR NKs active in the tumours and we're picking up these traces in the bloodstream. We don't know that yet. But it's interesting, and I think encouraging, that we're seeing these immune effects that have been seen with other immunotherapies at the time that we're infusing with the cells. And remember, this is the first dose level. And so to see these effects at this dose level, we take that as encouraging. Thanks. We have a few, a couple of questions related to the dose and the dose levels. So one question is, how many dose levels do we have in total? And another one is, Dose level 2 will use 3 times, 3 times as many cells as dose level 1. Based on what you have seen so far, what would you hope to see differently at the higher dose? Okay, so we have 3 defined dose levels in the protocol. There's also a 4th dose level that's not defined. That's a typical practice in protocols to give the flexibility in case you want to go in between dose levels or do something else. But 3 defined predefined dose levels. Dose level 2 is 3 times the exposure of dose level 1, and dose level 3 is 2 times the exposure of dose level 2, so 6 times the exposure of dose level 1. In terms of what we hope to see for dose level 2, I think very standardly with cell therapies and most other cell therapies, the higher the exposure, the more opportunity to see the effect. And so in broad terms, we would expect to see heightened effects of what we're beginning to see now in dose level 1. That's in broad terms. When we may expect to see very compelling clinical efficacy data is impossible to say at this stage, and it would be remiss for me to give a prediction of that. But what I will say is what we're seeing now is encouraging safety. and tickling and some immunological effects. And we continue to assess patients. We haven't completed the cohort. We continue to assess patients. But what we expect is to see heightened effects as we move up the dose levels. Thanks. And then one question related to recruitment. No patients were recruited in September, yet the company highlights ongoing recruitment efforts. What gives investors confidence that recruitment will accelerate going forward? It's a very good question. So with any clinical study and setup, the infrastructure needs to be established initially, and that happens at the time of activation and post-activation, actually. And so what we have now is we have built strong momentum in identifying patients across those 4 indications. As I say, over 30 patients that have been put through the initial screening cascade, so looking for MAJE-A4, and HLA-A2. It can take some time to build that momentum. And I think that has been actually, when compared to other studies, early phase studies, we have thankfully to, and thanks to the sites, we've actually swiftly moved to build that momentum. And now we can it wouldn't have been appropriate initially to estimate and guide on the rate of recruitment. But now we're in a position, as you have seen, in the presentation, to be able to guide on when we expect to fill the next cohort. And that's on the basis of the momentum that has grown. Over the last weeks since activation, weeks and short months, and the strong engagement of the sites to really consistently, continuously identify potential patients on the study. So I would say the confidence that the investors can have is in recognizing that we have over 30 patients. I think that's already a testament to how many patients have actually gone through the initial eligibility test, and that momentum continues and strong engagement continues. And hence, we expect to fill Cohort 2, of course, at a faster pace than Cohort 1. Thanks. So, just to practice. So, we're up and running, I'll say. Very good. Thanks. And just one practical question. Would you publish the full CIMA poster? Present at ESMO on our website. Both posters, ESMO and SITC, will be also presented tomorrow. That's a translational-leaning poster. ESMO was purely clinical. Both are on the design of the study and the plans for translational analysis and have no data presented at this stage. But both will be put onto the website. Thanks. Then one final question. You elaborated a little bit on it, but what is the significance of the recent external teaser clinical results for Zelluna? So this is a very important point, because what we have explained is the different levels of de-risking that we have been able to advance on account of really the great work of the team. And I think one element that has remained around the concept, since it's a novel differentiated concept, is whether the concept and the approach is able to drive responses in patients. And I think this external validation provides that piece. of information that demonstrates that a TCRNK is a different product for a different target and a different disease setting. But nonetheless, the approach itself Driving natural killer cells with T-cell receptors and targeting cancers that way has been demonstrated to work and drive deep response. in a myeloma patient, a complete response in a late-stage myeloma patient. If you like, that remains the one, had remained the one uncertain element around the concept. Can it work? And this data shows that it can. Thank you. I'm pleased to say we have answered all questions. And thank you all for participating at the call. And we hope you all enjoy the rest of your day. Thank you very much. Have a good day.