The process of EMT during which the fibroblasts transform into myofibroblasts by losing epithelial cell-related markers (such as E-cadherin, ZO-1) and gaining mesenchymal cell-related markers (e.g., α-SMA, N-cadherin, vimentin) (Thiery et al., 2009; Gonzalez and Medici, 2014) promotes the deposition of extracellular matrix, thus contributing to the development of pulmonary fibrosis. The gene discussed is ACTA1; the disease is pulmonary fibrosis.