Glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide (incretin) enhance β-cell insulin secretion and are therefore therapeutic targets for T2D treatment.(4) The effects of the so-called 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. This evidence concerns the gene GIP and type 2 diabetes mellitus.