In addition to a variety of improved treatment strategies in AML, the recognition that FLT3-ITD is an adverse prognostic marker, the integration of FLT3 inhibitors into the treatment algorithm, and the increased use of alloHSCT have led to improvements over the past 15 years in clinical outcomes in patients with FLT3-ITD-mutated AML. This evidence concerns the gene FLT3 and acute myeloid leukemia.