The anti-fibrotic effect of SGLT2 inhibitors is not limited to patients with diabetes; an animal study using unilateral ureteral obstruction, a typical renal fibrosis model, showed that use of an SGLT2 inhibitor inhibits fibrosis via a variety of fibrotic pathway-related mechanisms involving TGF-β1, αSMA, the Wnt cascade, CTGF, and fibronectin [25]. Here, CCN2 is linked to Ureteral obstruction.