For example, combined GLP-1 and GIP receptor deficiency is necessary to fully eliminate the glucose-lowering action of DPP-IV inhibition in mice15, β-cell responsiveness to both GLP-17–36 and GIP is increased in T2D patients with improved glycemic control16, and DPP-IV inhibition can partially restore the insulinotropic effect of GIP in T2D patients17. The gene discussed is GIP; the disease is type 2 diabetes mellitus.