Moreover, CaMKK2 directly phosphorylates Akt (protein kinase B) at Thr308 in addition to its canonical phosphorylation by PDK1 (phosphoinositide-dependent kinase-1), and the activation of the kinase activity of mTORC2 (mammalian target of rapamycin complex 2), which phosphorylates Akt at Ser473, results in the increased survival of tumor cells [88]. This evidence concerns the gene AKT1 and neoplasm.