SERPING1 and hereditary angioedema: However, regarding a possible pathophysiological explanation, it might be hypothesized that both C1-INH-HAE and FXII-HAE subgroups had a shared endothelial dysfunction that was probably not caused by C1-INH deficiency or mutated coagulation FXII per se, but instead by bradykinin receptor-ADMA pathway activation.