Because renal fibrosis and inflammation are two major pathological features determining the progression of DKD and are mediated by TGF-β/Smad3 and NF-κB signaling 2,14,17, we next examined whether overexpression of latent TGF-β1 inhibits renal fibrosis and inflammation by suppressing the TGF-β/Smad and NF-κB signaling. Here, SMAD3 is linked to diabetic kidney disease.