During EMT, biochemical changes occur in an epithelial cell, including the downregulation of epithelial markers like E-cadherin and the upregulation of mesenchymal markers such as N-cadherin and vimentin, giving it mesenchymal cell properties that allow it to spread, infiltrate and resist apoptosis, which may explain the aggressiveness of PSC. Also present in PSC are more and recurring genetic mutations compared to other pulmonary neoplasms [9]. This evidence concerns the gene CDH2 and lung neoplasm.