The epithelial–mesenchymal transition emerges as a pivotal regulatory mechanism, molecularly defined by transcriptional repression of the cell adhesion molecule E-cadherin coupled with concomitant induction of mesenchymal markers N-cadherin and vimentin, thereby conferring enhanced cellular motility and invasive capacity characteristic of aggressive tumor phenotypes [18,19]. The gene discussed is VIM; the disease is neoplasm.