GIP signaling is known to be dysregulated in diabetes, with tissues unable to respond to even supraphysiological doses of this hormone,21 and GIP is known to be normally anabolic to bone.18 Many mechanisms for the inhibition of GIP signaling in diabetes have been explored,21, 54 including desensitization of the GIPR with prolonged exposure to a ligand.55 Preliminary signaling studies (data not shown) did not suggest that a G‐protein receptor desensitization mechanism occurred in response to GIP in osteoblasts. This evidence concerns the gene GIP and diabetes mellitus.