C-terminally binding, pathogenic FH-autoantibodies described in aHUS or potentially pathogenic FH-autoantibodies in neuromyelitis optica spectrum disorder patients impaired the FH–C3b interaction [28,30,53,54,55], whereas non-pathogenic FH-autoantibodies in lupus nephritis patients did not influence C3b binding [56] and protective autoantibodies even increased C3-deposition in cancer patients [39]. The gene discussed is FH; the disease is neuromyelitis optica.