Exhibited high levels of renal Smad7 were associated with inhibition of renal Arkadia, suggesting that inactivation of the Arkadia-Smad7 ubiquitin proteasomal degradation pathway may be a key downstream mechanism through which latent TGF-β1 transgenic mice were protected against TGF-β/Smad3-mediated renal fibrosis and NF-κB-driven renal inflammation as previously reported 24-30. This evidence concerns the gene NFKB1 and renal fibrosis.