To block the TGF-β signaling at the level of its biosynthesis, antisense oligonucleotides (AONs) targeting the translation initiation of Tgfb1 mRNA have been used to repress ECM accumulation in rodent models of anti-Thy1 GN, diabetic nephropathy (DN), and UUO-mediated interstitial fibrosis 139-141. Here, TGFB1 is linked to diabetic kidney disease.