Our previous study showed that it was a potent inhibitor of idiopathic pulmonary fibrosis (IPF) and can regulate the expressions of α-smooth muscle actin (α-SMA) and epithelial cadherin (E-cadherin), two markers of the TGF-β/Smad (transforming growth factor beta/suppressor of mothers against decapentaplegic family) signaling pathway. Here, ACTA1 is linked to pulmonary fibrosis.