In the murine unilateral ureteral obstruction (UUO) model, depletion of M2 macrophages reduces renal fibrosis, and adoptive transfer of M2 macrophages promotes accumulation of myofibroblasts expressing smooth muscle α-actin [15] due to secretion of profibrotic factors like TGF-β, galectin-3, and FGF [16]. This evidence concerns the gene TGFB1 and renal fibrosis.