This model is Serping1 gene knockout mice, where the Serping1 gene homologous to the human SERPING1 gene has been knocked out. In Serping1 KO mice, C1-INH protein is deficient. This leads to a significant increase in vascular permeability, which closely mirrors the pathogenic mechanisms and clinical symptoms observed in human HAE patients. The homozygous mice are viable and fertile. Serping1 KO mice serve as valuable tools for studying the pathogenesis of HAE and screening therapeutic drugs.