based on the following evidence: (a) hyperglucagonemia is present in all forms of diabetes; (b) marked hyperglucagonemia is caused by perfusing anti-insulin serum to the normal pancreas; (c) during a total insulin deficiency, all metabolic manifestations of diabetes can be suppressed by glucagon suppressors, like somatostatin, and in global Gcgr knockout (Gcgr-/-) mice, demonstrating that β cell destruction does not cause diabetes (4). This evidence concerns the gene INS and diabetes mellitus.