Well, that’s a great question, and it’s kind of like right now we don’t know the answer. And the reason why we don’t know is because we don’t know how the plasticity of the cells change their profile and the proteomic surface under the selective pressure of the therapy. So we know how a tumor cell looks like before the therapy. But we don’t know after two weeks of CAR-T or bispecifics how that changes...
Well, that’s a great question, and it’s kind of like right now we don’t know the answer. And the reason why we don’t know is because we don’t know how the plasticity of the cells change their profile and the proteomic surface under the selective pressure of the therapy. So we know how a tumor cell looks like before the therapy. But we don’t know after two weeks of CAR-T or bispecifics how that changes. And we know it’s changing. There are studies showing that. So I guess the key for the future is to try to understand how this plasticity affects this tumor evolution. And if we know that there is, for example, a new target, let’s say a protein that is not expressed in myeloma, that after 10 days of this CAR-T is actually expressed, allowing the tumor to hide, then you have a new marker and you can get, for example, another CAR-T. So I think identifying this plasticity and how the cell transitions from one state to another will also allow us to identify new targets and eventually eradicate these dormant or frozen cells.
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