EMT plays a central regulatory role in pulmonary fibrosis, characterized by remodeling of alveolar-epithelial phenotypes, down-regulation of epithelial markers (e.g., E-cadherin) and up-regulation of mesenchymal markers (e.g., vimentin, N-cadherin), together with fibroblast-to-myofibroblast differentiation that establishes a pro-fibrotic micro-environment and drives disease progression (4). This evidence concerns the gene VIM and pulmonary fibrosis.