Consistent with previous studies that found that Smad2,Smad3,Smad4 and Smad7 might be involved in TGF-β1-mediated renal fibrosis [24–28], our study observed alterations in the phosphorylation activation of Smad2,Smad3,Smad4 and Smad7 in TGF-β1 treated HK-2 cells. Here, SMAD2 is linked to renal fibrosis.