Both loss of function mutations in the negative mTOR regulators such as phosphatase and tensin homolog (PTEN), tuberous sclerosis complex (TSC1/2), neurofibromatosis type 1 (NF1), liver kinase B1 (LKB1), also known as serine/threonine kinase 11 (STK11) and gain of function mutations in positive mTOR regulators such as AKT (also known as protein kinase B (PKB)) and phosphoinositide-3-kinase (PI3K) result in hyperactivity of mTOR signaling in a large number of malignant tumors [25,26]. This evidence concerns the gene AKT1 and cancer.