Consistent with this notion, CFHR1 and CFHR3 deficiency resulting from the CFHR1–3Δ has been associated with complement over-activation, increased inflammatory response, and increased risks of inflammation-related diseases, such as atypical hemolytic uremic syndrome (aHUS) and systemic lupus erythematous (SLE) [27], [28]. This evidence concerns the gene CFHR3 and atypical hemolytic-uremic syndrome.