The discovery that the insulinotropic properties of GLP-1 are preserved in human subjects with T2D [47] together with the capacity of GLP-1 to inhibit glucagon secretion, food intake, or gastric emptying, prompted the development of GLP-1 mimetics and inhibitors of GLP-1 degradation by dipeptidyl peptidase 4 (DPP4) for the treatment of T2D (reviewed in [48]). This evidence concerns the gene DPP4 and type 2 diabetes mellitus.