T2D pathogenesis involves several mechanisms that lead to impaired insulin secretion and function, including glucolipotoxicity (i.e., excess of glucose and long-chain free fatty acid levels in the plasma), oxidative stress (i.e., excessive production of reactive oxygen species and/or a deficiency in antioxidant defense systems), and endoplasmic reticulum stress (i.e., the endoplasmic reticulum protein folding capacity is overwhelmed). Here, INS is linked to type 2 diabetes mellitus.