This impairment, which is not the result of differences in glycaemia or insulinaemia during assessment, could contribute to the pathogenesis of hyperglycaemia in T2DM [8] and in particular to the reduction of early postprandial insulin secretion; in fact, the administration of GLP-1 receptor antagonists to healthy volunteers elicits both an impairment of meal-induced insulin secretion and an increase of postprandial glycaemia similar to that observed in T2DM. The gene discussed is GLP1R; the disease is Hyperglycemia.