AKT1 and neoplasm: FLT3-ITD was previously reported to synergistically activate the mTORC1/S6K/4EBP1 pathway through the PI3K/AKT and STAT5/PIM pathways to enhance eIF4F complex formation and promote the proliferation and survival of tumor cells, while FLT3-ITD is the most common tyrosine kinase mutation associated with poor prognosis in AML (54).