In view of the overwhelming evidence supporting the predominant role of bradykinin as the mediator of swelling in HAE and the absence of substantiating evidence for a kinin derived from C2,[32,38] it was of little surprise that drugs targeting bradykinin generation or action have shown efficacy in clinical trials for treatment of acute attacks of angioedema in HAE[40,41]. The gene discussed is KNG1; the disease is hereditary angioedema.