One of the key questions in HAE is the relationship between the hour-long angioedema effect of the short-lived BK production and the systemic plasmatic changes in the KKS activation process: the explanation might come from the cellular distribution of BK/desArg9-BK receptors and of membrane peptidases, and also from the persistence of circulating activated proteases [7]. The gene discussed is KNG1; the disease is hereditary angioedema.