SERPING1 and hereditary angioedema: The defect of C1INH can be either a quantitative deficiency (type I C1INH-HAE) or a qualitative dysfunction (type II C1INH-HAE) of the protein: the overproduction of bradykinin (BK) related to the lack of activity of C1INH leads to a consequent abnormal activation of the BK-B2 receptors (3) resulting in an increased vascular permeability and, thus, angioedema attacks (2).