Also, targeted deletion of its receptor, CXCR3, or administration of an anti-IP-10-neutralizing monoclonal antibody promoted renal fibrosis, without affecting macrophage or T cell infiltration in obstructed kidneys [96], thus suggesting that blockade of IP-10 via CXCR3 contributes to renal fibrosis, possibly by upregulation of transforming growth factor-beta1 (TGF-β1), concomitant with downregulation of hepatocyte growth factor (HGF). Here, TGFB1 is linked to renal fibrosis.