Bk-AE results from a variety of circumstances, such as a slow-down in bradykinin degradation subsequent to the use of angiotensin converting enzyme inhibitor (ACEI-AE), or the uncontrolled generation of bradykinin, such as observed in hereditary angioedema (C1-INH-HAE) and recurrent angioedema due to acquired C1-Inhibitor deficiency (C1-INH-AAE) [7] (Table 1). This evidence concerns the gene KNG1 and angioedema.