And so obviously, showing two months data is potentially uninformative. Four months data, usually all of those events have occurred in the past, and it has become clearer by four months, the trajectory for that patient. So four months data on a meaningful fraction of VAT in Q4 of this year. In terms of magnitude of ctDNA response, as I mentioned earlier, we’re powered to find the 20% delta, obviously, the higher the Delta, the more excited we will be. Because again, I think it’s truism that going down is good, and the more people you have going down, and the further down they go, and the more durable that decline in their ctDNA, the better. So it is a sliding scale. Greater frequency, depth and durability are all good. And we don’t yet have enough insight into how that correlates with overall survival to sort of think about boundaries, that just simply a quantitative qualitative statement, I think that more of that is a good thing.
Corinne Jenkins: That’s helpful. Thanks. And then. So with the SLATE candidate that you’re moving forward with it, I — It sounds to me like it’s slightly different versus when we thought as now, as you thought about updating that for next trial, just what were you trying to optimize for? And how do you think you’ve delivered that with this new, newer candidate?
Andrew Allen: Yes, it’s, we have tried to optimize, because obviously, one of the beautiful things about immunotherapy and the fact that we make our own products is that we can practice real translational development, whereby we observed in humans that in patients the outcomes, the effects of a particular vaccine, and we can then quickly iterate on it, and then hopefully improve it, make it and put it back in the clinic. It’s true. Bent bed to bench back to bed, biology and drug development, which is pretty exciting. And you’ve seen this with SLATE. If you remember, we have a version one of SLATE that contains KRAS mutations, but also some additional dead antigens. And what we observed there was that the magnitude of the immune response to the KRAS mutations was not as strong as we anticipated, based on preclinical testing under our GRANITE data.
And we dissected that out and realize that we actually had included an immune dominant antigen in the vaccine, which was a great antigen, but actually rare. And therefore, it didn’t, it wasn’t relevant to most patients. But it was presented by a common HLA alleles. And so many patients were making really strong immune responses to this dominant antigen. But those immune responses were useless because the tumor didn’t have the actual mutation. But the net effect was to actually then reduce the strength of the KRAS specific response, which is the one the patient needed. And so this was obviously a novel observation, no one had really understood the notion of a hierarchy of antigenic dominance within human cancer, new antigens. So this was a new observation, but an important one, and it was actionable.
So we modified the vaccine to remove that, that rare but dominant antigen, and we made a KRAS dedicated product. And that’s what we showed more data on that ESMO, last September in Paris. And we did indeed see a strong immune response to the modified vaccine exactly as we had intended. The key issues I mentioned earlier, is that we’re still delivering a single new antigen, and you just have to worry about acquired resistance. And the best way that we can deal with that is to deliver additional antigens relevant to the patient. And that’s the key term. It’s not enough, obviously, just to put in any old antigen, it has to be relevant to that patient’s tumor. And that’s the interesting question, what are those other antigens that that will be relevant to a patient with a KRAS mutation?
