AHUS is related either to a genetic deficiency in one or more soluble and/or membrane-bound complement regulatory proteins, usually Complement Factor H (CFH), or an acquired defect producing autoantibodies to complement-related factors, resulting in uncontrolled complement activation in the alternative pathway and thus inflammation of different blood vessels in the body [4,5]. The gene discussed is CFH; the disease is hyperinsulinemic hypoglycemia, familial, 4.