Serum levels and renal production of these cytokines are increased at the onset of renal disease (32, 34–37), and it has been described in murine models that the use of blocking antibodies against IFN-γ causes a significant delay in disease, stabilizing glomerulonephritis, and significantly decreasing proteinuria, which is associated with improvement in survival (36, 37). This evidence concerns the gene IFNG and glomerulonephritis.