Mainly, monocytic and FLT3-, RAS-, PTPN11- and TP53-mutated AML cells showed resistance to venetoclax caused by higher levels of MCL-1, suggesting that these subgroups of AML cases could be efficiently treated with the combination of venetoclax and a MCL-1 inhibitor [97,100]. The gene discussed is TP53; the disease is acute myeloid leukemia.