Animal studies revealed that overexpression of an active form of TGF-β1 in liver led to progressive kidney fibrosis in mice (Kopp et al., 1996), whereas overexpression of latent TGF-β1 in the skin displayed anti-inflammatory and anti-fibrosis effects in obstructive and crescentic glomerulonephritis (Huang et al., 2008a, b). This evidence concerns the gene TGFB1 and crescentic glomerulonephritis.