We have previously shown that glomerular disease in the mouse model of anti-GBM-GN is accompanied by oxidative damage as shown by increased levels of malondialdehyde and H2O2, upregulation of myeloperoxidase and NADPH oxidase, downregulation of catalase and glutathione peroxidase, increased levels of nitrotyrosine, activation of NFkB, upregulation of inducible nitric oxide synthase and osteopontin expression, and decreased PPARγ expression [17]. Here, NFKB1 is linked to glomerular disorder.