The role of glucagon in contributing to hyperglycemia in diabetes was reinforced by observing lower glucose levels in mice whose expression of the glucagon receptors (GCGRs) has been knocked out [74], as well as by the improved glucose and HbA1c levels in humans treated with acute and prolonged pharmacological receptor antagonists (GRAs) in clinical and preclinical trials, although these were accompanied by hepatic side effects such as increases in transaminases, liver fat accumulation, and dyslipidemia in addition to α-cell hyperplasia [75,76,77]. The gene discussed is GCGR; the disease is metabolic syndrome.