Acquired forms of BMAE include angiotensin converting enzyme (ACE) inhibitor-induced AE, AE due to acquired C1–INH deficiency, and acquired idiopathic non-histaminergic AE; while the former is due to reduced catabolism of bradykinin, the latter is due to consumption of C1–INH by the neoplastic lymphatic tissues and/or anti-C1-INH neutralizing autoantibodies.3 This evidence concerns the gene SERPING1 and hyperinsulinemic hypoglycemia, familial, 4.