Moreover, inhibition of Kv7.1 and Kv11.1 increases the glucose-stimulated insulin and C-peptide secretion from the pancreatic beta cells and increases glucagon-like peptide (GLP)-1 in mice [2, 3] and we have previously shown that patients with LQT1 (due to loss of function mutations in KCNQ1) and LQT2 (due to loss of function mutations in KCNH2) have glucose-stimulated hyperinsulinemia and postprandial hypoglycaemia [2, 4]. This evidence concerns the gene KCNH2 and hyperinsulinism.