Characterized by the down-regulation of epithelial markers (e.g., E-cadherin) and the up-regulation of mesenchymal markers and EMT-specific transcription factors (e.g., Vimentin, N-cadherin, and Snail), EMT is widely regarded as an important initiator and driver of pulmonary fibrosis and its complications, where alveolar epithelial cells are exposed to profibrotic signals, such as transforming growth factor-beta (TGF-β), begin to lose their epithelial characteristics and acquire a mesenchymal phenotype (12). This evidence concerns the gene TGFB1 and pulmonary fibrosis.