In the setting of insulin resistance, two important pathological defects lead to type 2 diabetes which include: (1) decreased ability of insulin to act on peripheral tissues to stimulate glucose metabolism or inhibit hepatic glucose output; and (2) inability of the pancreatic beta cells to fully compensate for the degree of insulin resistance in genetically predisposed individuals, leading to a state of relative insulin deficiciency [11,14,15]. This evidence concerns the gene INS and type 2 diabetes mellitus.