Potential mechanisms for the CRC anticancer effect of MET include activation of AMPK/inhibition of mTOR, inhibition of the PI3K, and mitogen-activated protein kinase (MAPK) signaling pathways, lowering of hyperinsulinemia, inhibition of cellular respiration through inhibition of respiratory complex I, and modulation of inflammatory response [3,4,5,14,58,59]. The gene discussed is MTOR; the disease is hyperinsulinism.