Genetically deficient or medically antagonized CCR2 led to decreased macrophage infiltration and renal fibrosis, as well as decreased expression of CCL2, type I collagen, and TGF-β expression [42]; another study showed that CCR2 knockout mice accumulated fewer bone-marrow derived myofibroblasts and a lower expression of α-SMA and FSP-1 in obstructed kidneys [11]. This evidence concerns the gene TGFB1 and renal fibrosis.