While targeted therapies, such as FLT3 inhibitors or the BCL-2 inhibitor venetoclax, are either directly addressing a constitutively active receptor tyrosine kinase identified by mutational analysis, or inhibiting an important anti-apoptotic protein in defined clinical setting, the biology of AML with MLL- (KMT2A) rearrangement (KMT2Ar) is almost unique and therapeutic strategies are more complex [127]. This evidence concerns the gene FLT3 and acute myeloid leukemia.