FLT3 and acute myeloid leukemia: According to the hypothesis of the simplified “two-hit model of leukemogenesis”, in many cases, two types of mutations are involved in AML pathogenesis: one resulting in uncontrolled proliferation (e.g., FLT3, NRAS) and the other leading to impairment of physiological myeloid differentiation (e.g., TP53, CEBPA) [2].