AKT1 and acute myeloid leukemia: Functionally, aberrant Wnt/β-catenin and/or phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mechanistic target of rapamycin signaling, frequently implicated in the pathogenesis of AML, has also been shown to suppress autophagy, resulting in low differentiation ability [578,579].