SF3B1-mutated AML has been identified as a marker of venetoclax resistance [101], and it remains to be seen whether HMA–venetoclax, especially decitabine–venetoclax (since SF3B1-mutated AML appears to be particularly sensitive to decitabine-based therapy) [102], can overcome resistance through a synergistic effect [103]. This evidence concerns the gene SF3B1 and acute myeloid leukemia.