However, new mechanisms are reformulating the pathophysiological concept of T2DM, for example, the defect in the incretin system (Glucagon-like peptide-1 or GLP-1, and Gastric inhibitory polypeptide or GIP), promoting hyperglycemia by less stimulation of insulin secretion by pancreatic beta-cells, and less suppression of glucagon release by pancreatic alpha-cells[1]. This evidence concerns the gene GIP and Hyperglycemia.