The dual inhibition of protein kinases in AML has been extensively explored to achieve response to relapsing and resistant tumors avoiding toxic side effects, mainly involving co-inhibition of the phosphatidylinositol 3-kinase(PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) (PI3K/AKT/mTOR) pathway and FLT3 kinase. Here, AKT1 is linked to acute myeloid leukemia.