For example, activation of the alternative complement pathway is required to induce vascular inflammation in AAV.[4] In renal tissue of AAV patients with positive MPO-ANCA, C3d, and factor B co-localized with MAC, the involvement of an alternative pathway of complement system was thus suggested.[17] In addition to roles of MAC, it is reported that C5a mediates ANCA-induced glomerulonephritis[18] and that C5a receptor blockade protected against MPO-ANCA-induced glomerulonephritis in a murine model.[19]. This evidence concerns the gene C5 and glomerulonephritis.