Deletion of CFB (−/−) has been shown to rescue the renal phenotype in CFH KO mice (that exhibit a C3G-like pathology due to uncontrolled AP activation) and leads to a less severe renal disease and immune complex deposition in LN disease models, highlighting the critical role of FB in driving the AP/amplification loop and in the pathophysiology of complement-mediated diseases (55–57). The gene discussed is CFB; the disease is kidney disorder.