According to Williams et al., a lipophilic statin, i.e., fluvastatin, can decrease the mutant FLT3’s kinase activity via preventing advanced glycosylation of the receptor, reducing FLT3-ITD cell surface expression, inhibiting the activation of MAPK and AKT, and reducing the TKI drug resistances while leading to the apoptosis of FLT3-ITD-mutated AML cells [68]. This evidence concerns the gene AKT1 and acute myeloid leukemia.