Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive inflammatory disease of the interstitial lung, and transformation of myofibroblast from fibroblast is a hallmark of IPF.1 During the development of IPF, myofibroblast not only expresses α‐smooth muscle actin (α‐SMA), but also produces extracellular matrix (ECM) production, such as type I collagen, leading to the IPF.2 Epithelial‐to‐mesenchymal transition (EMT) is highlighted as an important, possible mechanism of IPF. The gene discussed is ACTA1; the disease is idiopathic pulmonary fibrosis.