In a mouse model using injection of anti-MPO IgG as an inducer of glomerulonephritis (GN), the development of crescentic GN was prevented in mice deficient of C5 (common complement pathway) and factor B (alternative complement pathway), while mice lacking C4 (classic and lectin complement pathways) developed disease to the same extent as wild-type mice [8]. This evidence concerns the gene C4A and ganglioneuroma.