How do I know what my risk of relapse is?

A very, very important question. And the question, the answer to that is evolving. The more we know about the disease biology, the more we can refine the risk of relapse. But in general, if we try to divide it into two groups. One is the features that are present at diagnosis or the pre-treatment features. And the second group we talk about the post-treatment features. For pre-treatment features, the risk categorization is possibly the most important thing. For AML, when we risk categorize it, we mostly base on the chromosomal abnormalities. And more recently, we're also including the mutational pattern in defining the risk stratification. So then you can define it by the European Leukemia Network. They have defined it into three groups. The favorable, intermediate, and high risk. Now the intermediate risk, you can divide it into intermediate one or intermediate two. But those are more specifics, but in general. So those are the information that are incorporated. The chromosomal abnormality, number one. And number two, the mutation profile in defining the risk categorization. That possibly is the most important pre-treatment feature that defines the risk of relapse. Now the other possibilities are if there are organ dysfunctions, coexisting organ dysfunctions. Now they not only can increase the risk of mortality from the induction treatment, but at the same time, because of the compromise on the intensity of treatment, because if you have, say, a kidney dysfunction, you might want to compromise on the dose of the chemotherapy. Same thing is true if there is a liver dysfunction. So sometimes organ dysfunctions also dictate what intensity of treatment we can use. And if we cannot use the most optimal intensity of treatment, that also increases the risk of relapse. So those are more of the pre-treatment feature. Now the after treatment, when we assess for response, one thing that matters quite a lot is the quality of response. There are different categorizations of response. You call it complete remission, complete remission with incomplete platelet recovery, complete remission with incomplete recovery of counts, or quote unquote CRP, CRIs. Of all the responses, achieving a complete remission is possibly something extremely important because that's a good quality remission. And that matters in the long run in terms of the disease coming back. Now we've been able to refine this a little more, mostly by use of minimal residual disease evaluation, whether you do it by flow cytometry or if there are certain mutations that are present at diagnosis, those mutations can be tracked over time. So you can define minimal residual disease or measurable residual disease either by flow cytometry or by mutation profiling. And most are relevant in the appropriate context. So that's the depth of response. Complete remission is more by morphologies looking under the microscope, counting the blast and the blood count recovery, whereas the flow cytometry-based minimal residual disease or mutation-based minimal residual disease, it's a deeper dive into the quality of response. Those matter. Now, if you had abnormal chromosomes at the beginning, the abnormal chromosomes disappearing, that matters. So those are the post-treatment features that mostly are important in kind of predicting what are the general chances of relapse.