SERPING1 and hereditary angioedema: Although HAE follows an autosomal dominant inheritance pattern, approximately 25% of cases arise from de novo mutations.[12] Among the 748 known type II HAE mutations, 70% involve substitution of arginine 466 with cysteine or histidine, rendering C1-INH nonfunctional.[12] In our case, we identified a c.1397G > A (p.Arg466His) mutation in the proband; subsequent family screening detected 3 additional affected individuals, enabling early intervention and potentially reducing the risk of fatal complications.