FLT3 and acute myeloid leukemia: FLT3-ITD mutation can lead to constitutive autophosphorylation of FLT3 and activation of its downstream effectors including RAS/RAF/MEK, MAPK/ERK, PI3K/AKT, and JAK/STAT signal pathways, result in uncontrolled cell proliferation, survival, and differentiation of AML, while FLT3-ITD inhibitors can inhibit these downstream pathways through specific FLT3 inhibition [16].