TGF-β1/Smad3 signaling also drives Endothelial to Mesenchymal transitions (EndoMT), where smad3 inhibitor and endothelium-specific TGF-β receptor knockout reduces EndoMT mediated diabetic nephropathy in streptozotocin (STZ)-induced diabetes and tubulointerstitial fibrosis in unilateral ureteral obstruction models in vivo (68, 69). This evidence concerns the gene SMAD3 and diabetic kidney disease.