Hereditary angioedema. Type I and II are caused by a mutation in the SERPING1 gene that makes the C1 inhibitor protein.

https://en.wikipedia.org/wiki/Hereditary_angioedema

Therapeutic effect of danazol may have two mechanisms of action: (1) promotion of C4 synthesis by anabolic effect resulting in an improvement of the complement system with the disappearance of CIC and (2) a minor increase in C1 inh level primarily due to the lack of its consumption.

Most cases of HAE are caused by mutations of the SERPING1 gene, which contains the information necessary to generate a protein called C1 esterase inhibitor (C1INH). People with HAE produce nonfunctional or insufficient amounts of C1INH, leading to spontaneous swelling in the body. As a consequence of C1INH deficiency, C4 protein levels are also almost always low in HAE patients.

Winstrol = Stanozolol increases levels of C1INH and C4 protein in the blood by enhancing their production. Elevating levels of the two proteins close to the normal range helps prevent HAE attacks. Although the exact mechanism of how it acts on protein production is not fully understood, Winstrol is a well-established treatment for managing HAE.

FA 2018 page 107

C1 esterase inhibitor deficiency: Causes hereditary angioedema due to unregulated kvllikrein activation, which leads to increased bradykinin.

There are three main types of HAE.[3] Type I and II are caused by a mutation in the SERPING1 gene that makes the C1 inhibitor protein while type III is often due to a mutation of the factor XII gene.[3] This results in increased amounts of bradykinin which promotes swelling.[3] The condition may be inherited from a person's parents in an autosomal dominant manner or occur as a new mutation.[3] Triggers of an attack may include minor trauma or stress, but often occurs without any obvious preceding event.[3] Diagnosis of type I and II is based upon measuring C4 and C1-inhibitor levels.