Experimental studies have shown that inhibition of endogenous CCN2 by antisense oligonucleotides slows disease progression in experimental diabetic nephropathy, unilateral ureteral obstruction, and nephrectomized TGF-β1 transgenic mice [3, 12–14], suggesting that selective CCN2 blockade could be used to treat renal disease. This evidence concerns the gene CCN2 and Ureteral obstruction.