FLT3 and acute myeloid leukemia: Many AML-associated mutations are clearly linked to one of these categories, such as constitutive activation of RAS proteins or FLT3, that drive uncontrolled proliferation (1–3), mutations that prevent cell cycle arrest and apoptosis such as TP53 (4), and mutations that hinder differentiation such as in the transcription factors RUNX1 or C/EBPα (5, 6).