Mesenchymal cells change profoundly during the pathogenesis of lung fibrosis, and our results indicate that KLF4, a key regulator of cell transitions, is profibrotic in PDGFR-β+ cells and, through noncell autonomous effects, is antifibrotic in SMA+ cells (Figs. 3 and 5). This evidence concerns the gene PDGFRB and pulmonary fibrosis.