Despite diverse initiating insults, glomerulosclerosis and tubulointerstitial fibrosis are pathological features common to most forms of progressive renal disease. Control of systemic hypertension and blockade of the renin-angiotensin system ameliorate the rate of progression of chronic renal disease; however they generally fail to completely arrest the scarring process. While the chain of events leading to scarring are still being defined, TGF-beta is a cytokine that plays a pivotal role in the pathogenesis of glomerulosclerosis and tubulointerstitial fibrosis . Given the pleiotropic effects of TGF-beta, significant attention has focused on the potential of its downstream mediators as therapeutic targets. Connective tissue growth factor (CTGF) is a member of the CCN gene family, which includes CyR61 (cysteine rich 61), Nov (Nephroblastoma overexpressed) and the WISP family (for review see [2,3,4]). These immediate-early genes coordinate complex biologic processes during differentiation and tissue repair . Increased expression of CTGF has been detected in experimental and human renal fibrosis where it correlates with glomerulosclerosis and the degree of tubulointerstitial fibrosis . In these settings CTGF expression is regulated at least in part by TGF-beta. This review details the biology of CTGF with specific reference to its potential as a therapeutic target in renal fibrosis.