However, recent studies have demonstrated that simultaneous treatment with FLT3 inhibitors, which potentially block mutational PI3K/AKT downstream signaling, significantly improved therapeutic efficacy of: (1) HMAs in elderly/unfit FLT3 mutant AML patients (azacytidine/gilteritinib); and (2) standard AML chemotherapy in younger FLT3 mutant AML patients (cytarabine/anthracycline/midostaurin or cytarabine/anthracycline/quizartinib) [Table 2][73-75]. The gene discussed is AKT1; the disease is acute myeloid leukemia.