For example, nondiabetic patients treated with somatostatin analogs for growth hormone excess frequently develop hyperglycemia due to insulin suppression.3,4 Meanwhile, in insulin-dependent patients with diabetes, somatostatin and somatostatin analogs prevent DKA5 and improve both postprandial hyperglycemia6–9 and morning hyperglycemia10 by suppressing glucagon. This evidence concerns the gene INS and Hyperglycemia.