These findings complement the clinical features associated with CTLA‐4 deficiency in humans,36 and previous observations that CTLA‐4 deficient mice develop autoimmunity,35 as well as high soluble serum levels (ie, low cell surface expression) in patients with myasthenia gravis.37 The gene discussed is CTLA4; the disease is hyperinsulinemic hypoglycemia, familial, 4.