In terms of the HK-gC1qR relationship, a critical association that mediates inflammation and vascular permeability, structure-function studies involving gC1qR deletion mutants demonstrated that domains 190–202 and 204–218 on the receptor are involved in an HK binding pocket (Ghebrehiwet et al., 2011) that represents a prospective therapeutic target for post-AIS cerebral edema. The gene discussed is KNG1; the disease is androgen insensitivity syndrome.