From what we know now, for example, the availability of BCMA is a target on plasma cells in patients who have not been exposed to a BCMA-directed therapy is quite high. So it’s unlikely that patients will not express, well, the myeloma cells will not express BCMA and therefore the need to test for BCMA expression before starting the BCMA therapy in a patient that is BCMA naive is probably, at least for what we know now, not that relevant...
From what we know now, for example, the availability of BCMA is a target on plasma cells in patients who have not been exposed to a BCMA-directed therapy is quite high. So it’s unlikely that patients will not express, well, the myeloma cells will not express BCMA and therefore the need to test for BCMA expression before starting the BCMA therapy in a patient that is BCMA naive is probably, at least for what we know now, not that relevant. GPRC5D is a similar argument, I would say, although losses may be seen even in patients who have not been exposed. But I would say for now, a marker is not on the horizon yet, but there are platforms that are allowing us to actually assess the presence of both BCMA and GPRC5D. And also, their mutations because we know that not only the expression matters, but also mutations. So potentially in the future, we will be able to answer this question also in the clinic. And I would say that more importantly than when patients are treated for the first time with these agents, this matters in terms of retreatment. So after a patient has been exposed, for example, to a CAR-T, does it make sense to move forward and relapse with another BCMA agent that is, for example, a bispecific antibody? Well, we need to check for BCMA expression, their mutations, and make sure that this is really relevant, or maybe changing the target makes more sense.
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