Yue and colleagues [246] demonstrated using high-dose STZ-injected diabetic rats subjected to a hypoglycemic clamp that the attenuated glucagon response to insulin-induced hypoglycemia could be significantly improved by the simultaneous application of a SSTR2 antagonist (SSTR2a), confirming an elevation in basal somatostatin release and paracrine feedback inhibition on the alpha-cells. The gene discussed is SST; the disease is Hypoglycemia.