These mechanisms include the amplification or mutation of genes encoding PI3K subunits, AKT, and other pathway members; the activation of receptor tyrosine kinases, mutation, or overexpression of growth factor receptors, e.g., epithelial growth factor receptor (EGFR) or human epidermal growth factor receptor 2 (HER2); the inactivating mutations in the genes encoding key tumor suppressors PTEN or INPP4B; the inactivating mutations in the genes encoding mTOR regulators such as TSC1 and TSC2; and the activating mutations in MTOR itself [91,92,93]. This evidence concerns the gene MTOR and neoplasm.