The pathophysiology of ACE-induced angioedema is attributed to the accumulation of bradykinin, which is a potent vasodilator with proinflammatory activity that is normally degraded by angiotensin-converting enzyme (ACE), aminopeptidase P (APP), neutral endopeptidase (NEP), dipeptidyl peptidase-4(DDP-4), and kininase I. The five-membered nitrogen heterocycles in certain ACE inhibitors may enhance bradykinin release, leading to increased vascular permeability and subsequent angioedema [15]. This evidence concerns the gene MME and angioedema.