Remarkably, compared with control group, TGF-β1 treatment activated not only Smad2 and Smad3, but also p38 MAPK with a concomitant expression of α-SMA in both donor and IPF fibroblasts, while PM014 co-treatment resulted in a dose-dependent suppression of TGF-β1 signaling pathway stimulating EMT. This evidence concerns the gene SMAD2 and idiopathic pulmonary fibrosis.