Zhou et al. found AA-induced progressive renal failure and tubulointerstitial fibrosis in Smad3 wild type mice, but not in Smad3 knockout mice, indicating that Smad3 is a key factor in the development of AA-induced nephropathy (Figure 1) and that the specific deletion of TGF-β/Smad3 signaling may be a potential therapeutic target for chronic AAN [62]. This evidence concerns the gene SMAD3 and Nephropathy.