Our results have demonstrated that genetic deletion of CXCL16 protects the kidney from angiotensin II infusion-induced renal dysfunction, inhibits renal fibrosis, reduces proteinuria, suppresses bone marrow-derived fibroblast accumulation, myofibroblast formation, macrophage, and T cell infiltration and pro-inflammatory cytokine expression without affecting blood pressure at baseline or in response to angiotensin II infusion (Xia et al., 2013b). Here, AGT is linked to renal fibrosis.