The pathogenic manifestations of Nrf2 knockout mice were inflammatory lesions in multi-organ, intravascular deposition of immunoglobulin (Ig) complexes and premature death due to rapidly progressing glomerular nephritis (47), in response to pro-inflammatory condition, suggesting that Nrf2 has a critical role in noxious stressors and cellular adaptation. This evidence concerns the gene NFE2L2 and glomerulonephritis.