While the complement system is typically activated through the classic pathway and the lectin pathway, the CFB-regulated alternative pathway plays a significant role in the pathogenesis of kidney diseases, such as lupus nephritis (13, 14), atypical hemolytic uremic syndrome (15, 16), complement 3 (C3) glomerulopathies (GNs) (17), anti-neutrophil cytoplasmic antibody–associated (ANCA-associated) GN (18, 19), autosomal dominant polycystic kidney disease (ADPKD) (20), IgA nephropathy (21), and immune rejection after renal transplantation (22). This evidence concerns the gene CFB and atypical hemolytic-uremic syndrome.