The m6A epitranscriptomic regulators are not uniformly dysregulated per cancer type. Just like there are subsets of cancer types that express HER2, VEGFR, or are sensitive to immunotherapy, there are going to be cancer types that express FTO or writers at higher or lower levels to drive tumorigenesis.
Fortunately for Bisantrene and unfortunately for someone trying to understand the complete addressable market, it has multiple mechanisms of action, which means it is not just limited to cancer types that are sensitive to FTO inhibition. I believe we are going to be made more aware of these mechanisms early next year.
You also have interesting things like the paper below to add to the confusion where FTO was downregulated in this cancer type and silencing led to tumorigenesis, but also sensitized the therapy to synergy treatment.
Pillar 1 - FTO (new thread), page-3009
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