Accelerated models of anti-GBM glomerulonephritis induced in FcγRI−/−, FcγRIII−/− and FcRγ−/− mice have demonstrated that FcRγ, especially FcγRIII, plays a pivotal role in the pathogenesis through the antibody-dependent pathway [13]. This evidence concerns the gene FCER1G and glomerulonephritis.