INS and hyperinsulinism: The central role of KATP channels in insulin secretion and glucose homeostasis is underscored by dysregulated insulin secretion and blood glucose in humans bearing KATP mutations: loss-of-function mutations cause congenital hyperinsulinism characterized by persistent insulin secretion despite life-threatening hypoglycemia8,9; conversely, gain-of-function channel mutations result in neonatal diabetes due to insufficient insulin secretion10.