Consequently, a repair process driven by TGF-β1 induces a switch of M1 macrophages towards an M2 pro-fibrotic phenotype.29, 30, 31, 32, 33 A key component in this repair process is TGF-β1/Smad3-driven MMT,17, 34, 35 which induces the transition of M2 macrophages into collagen-producing α-SMA+ myofibroblasts which contribute to the excessive deposition of extracellular matrix occurring during renal fibrosis. This evidence concerns the gene ACTA1 and renal fibrosis.