In contrast to the active form of TGF-β1, the latent form of TGF-β1 can protect the kidney against fibrosis and inflammation by upregulating Smad7 that is observed in the latent TGF-β transgenic mice received with UUO-induced nephropathy or anti-GBM-induced glomerulonephritis (Huang et al., 2008a,b). This evidence concerns the gene TGFB1 and Nephropathy.