The incretin response is thought to be defective in T2D, manifesting in part with a complete lack of β-cell responsiveness to exogenously administered GIP.6,8 The β-cell maintains responsiveness to exogenously administered GLP-1, but the response may be somewhat attenuated compared with that seen in the non-diabetic state, indicating a partial incretin defect with GLP-1.9 Due to these effects on the β-cell, GLP-1 became an attractive pharmacologic target, and harnessing it in some fashion was enticing. This evidence concerns the gene GIP and type 2 diabetes mellitus.