One promising target for molecular therapy in AML is the phosphatidylinositol 3-kinase (PI3K)/Akt/mechanistic target of rapamycin (mTOR) signaling pathway, which is constitutively activated in 70-90% of AML patients and has been shown to be central to the proliferation, survival, and drug-resistance of leukemic cells [8, 9]. Here, AKT1 is linked to acute myeloid leukemia.