Adherens junctions are disrupted, and their components such as E-cadherin, β-catenin, p120-catenin and α-catenin are often downregulated and/or dissociated, whereas mesenchymal cell markers including N-cadherin, vimentin and fibronectin are upregulated.2 EMT increases cell plasticity and motility, thereby permitting tumour cells to leave their original sites, enter the systemic circulation, and reconstruct tumours at distant sites.4 The development of therapeutic measures to inhibit EMT would therefore be of paramount importance for prevention of cancer metastasis. The gene discussed is CDH1; the disease is neoplasm.