Of note, such disease-associated C3 variants are thought to drive HUS pathology, in the context of an overall compromised complement regulatory landscape (i.e., presence of at-risk CFH and MCP haplotypes), and consequent to a priming event that makes the renal endothelium more susceptible to C3 deposition and inflammatory damage (26, 29). The gene discussed is CFH; the disease is hemolytic-uremic syndrome.