Additionally, Loeffler et al. have demonstrated that S100A4 (FSP1)-specific Smad2 knockout in the kidney attenuates fibrosis and mitigates epithelial-to-mesenchymal transition in mice with diabetic nephropathy induced by STZ through suppression of TGF-β1 and Smad3 protein expression [48]. This evidence concerns the gene TGFB1 and diabetic kidney disease.