It reduces the binding of GCGR and glucagon and insulin secretion; this observation led Hansen to hypothesize that the Gly40Ser mutation in GCGR can lead to the abnormal functioning of islet β cells and may predispose carriers to diabetes, possibly by impairing glucagon-mediated signaling and decreasing the sensitivity of the target tissues to glucagon (64). The gene discussed is GCGR; the disease is diabetes mellitus.