Conversely, conditional deletion of Smad4 in podocytes attenuated DKD in diabetic eNOS-deficient mice 62, and global Smad3 loss also protected from podocyte injury caused by high fat diet-induced obesity in mice 63, further corroborating the importance of podocyte TGF-β signaling in promoting diabetic glomerulopathy. Here, TGFB1 is linked to diabetic kidney disease.