Glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide (incretin) enhance β-cell insulin secretion and are therefore therapeutic targets for T2D treatment.(19) The effects of ominous octet (increased lipolysis, glucose reabsorption, hepatic glucose production in the liver, and glucagon secretion; decreased glucose uptake, insulin secretion, and incretin levels; and neurotransmitter dysfunction) lead to hyperglycemia in T2D. Here, INS is linked to Hyperglycemia.