In the unilateral ureteral obstruction-induced pulmonary fibrosis model, 30% of myofibroblasts were CD68+ and α-SMA+, and alternatively activated macrophages were shown to directly transdifferentiate into collagen-producing α-SMA+ myofibroblasts via TGF-β/Smad3 signaling [113,119,125,126,127,128]. This evidence concerns the gene ACTA1 and pulmonary fibrosis.