Due to gain-of-function mutations of proto-oncogenes such as epidermal growth factor receptor (EGFR), PI3K, and AKT, or loss-of-function mutations of tumor suppressors, such as phosphatase and tensin homolog deleted from chromosome 10 (PTEN), tuberous sclerosis complex 1 (TSC1), and tuberous sclerosis complex 2 (TSC2), mTORC1 is frequently activated in human cancers 4, 5. The gene discussed is AKT1; the disease is neoplasm.