For example, diabetic kidneys of Ccl2-deficient mice or those treated with Ccl2 inhibitors had reduced macrophage infiltration, reduced myofibroblast accumulation and ameliorated renal fibrosis78,79, suggesting that Ccl2-mediated macrophage accumulation contributed to myofibroblast activation and renal fibrosis. Here, CCL2 is linked to renal fibrosis.