AKT1 and neoplasm: Studies have demonstrated that insulin activates the phosphoinositide 3-kinase-protein kinase B-mammalian target of rapamycin (PI3K-Akt-mTOR) and RAS-mitogen-activated protein kinase (RAS-to-MAPK) pathways by binding to the cognate receptor or insulin-like growth factor receptor, which in turn can lead to downstream cellular proliferation and protein synthesis in tumor cells.