AKT1 and cancer: In human cancers, overexpressed or hyperactivated via oncogenic mutation receptor tyrosine kinases (RTKs), phosphatidylinositol-3 kinase (PI3K), and v-akt murine thymoma viral oncogene (AKT), as well as small GTPase (RAS) and mitogen-activated protein kinase (MAPK) signaling pathways, converge to activate mTORC1 (Figure 1).