Renal fibrosis in these models is also strongly associated with the presence of M2 macrophages (79–83); in fact, adoptive transfer of M2 macrophages after unilateral ureteral obstruction (UUO) promoted the accumulation of αSMA+ cells (indicative of fibrotic scarring), a phenotype that involved signaling by members of the TGFβ superfamily (84). This evidence concerns the gene TGFB1 and renal fibrosis.