AKT1 and neoplasm: Gain-of-function mutation in Ras, Raf, PI3K and AKT (activating mutation) oncogenes and loss-of-function mutations in the TSC, PTEN (phosphatase and tensin homolog) and neurofibromatosis-related protein-1 may lead to constitutive activation of mTORC1 that results in anabolic processes driving tumor cell growth and proliferation [107].