Since mutation status was not available at the time of treatment, all therapeutic approaches employed in this study were “mutation status blind.” Subsequent to the conduct of the clinical treatment of the patients, a genetic cause of CHI due to mutations in the ATP-sensitive K+ channel subunits (KCNJ11 and ABCC8) was identified in 10 patients. Here, ABCC8 is linked to congenital isolated hyperinsulinism.