Pirfenidone prevented changes in the fibrotic fibroblast phenotype such as increase in proliferation and migration and elevation in the levels of phospho-Smad3, phospho-signal transducer and activator of transcription 3 (STAT3), α-SMA, and collagen in the context of IPF [39]. The gene discussed is ACTA1; the disease is idiopathic pulmonary fibrosis.