Certainly, EMT in clinical cancer specimens is defined as loss of junctional E-cadherin; switch to other cadherins (e.g., N-cadherin); degradation of cell–cell adhesion; apicobasal polarity and tissue architecture; pleiotropic cell shape; nuclear β-catenin, Snail or Slug expression; and otherwise unexpected expression of mesenchymal markers such as vimentin (Thompson et al, 2005). The gene discussed is SNAI2; the disease is cancer.