The insulin-deficient Gcgr−/− mice did not become hyperglycemic or hyperketonemic, and their livers exhibited no increase either in phosphor-cAMP response element-binding protein (p-CREB); a mediator of glucagon action (Altarejos and Montminy, 2011) or in the gluconeogenic enzyme phosphoenolpyruvate carboxykinase, both of which are elevated in uncontrolled diabetes. Here, GCG is linked to diabetes mellitus.