The mechanisms that contribute to increased risk in diabetes and hyperglycemia are poorly understood but likely are related to insufficient activation of pro-survival signaling pathways, elevated nitrosative stress, activation of the PI3K/Akt/mTOR (phosphatidylinositol 3-kinase, serine/threonine kinase also known as protein kinase B, and mammalian target of rapamycin) pathway, and autophagy46. This evidence concerns the gene MTOR and diabetes mellitus.