Acute myeloid leukemia (AML) is a heterogeneous malignancy characterized by proliferating myeloblasts in the bone marrow.1 Abnormal or constitutive signaling through various intracellular pathways is often observed in AML cells, including activation of the phosphatidylinositol 3-kinase (PI3K)-Akt-mechanistic target of rapamycin (mTOR) pathway.2 Its activation can be initiated by various mechanisms, including cell adhesion molecules, oncogenes, mutated receptor tyrosine kinases, G-protein-coupled receptors (GPCRs), and other cytokine receptors.2 This evidence concerns the gene AKT1 and acute myeloid leukemia.