Other investigations using an animal model suggested that complements may contribute to the pathogenesis of anti-GBM disease; it was confirmed that the reduction in the severity of nephritis induced with anti-GBM serum was mild in C4-deficient mice [160], moderate in C3-deficient mice [C14], and greater in mice deficient in both C3 and C4 [161]. This evidence concerns the gene C3 and nephritis.