Since the initial description of the E-cadherin repressor SNAI1 as potential mediator of a more aggressive tumor phenotype [35], several studies have examined the potential consequences of EMT in SCC of the head and neck (HNSCC) in vitro [36-38] and in vivo [25,26,32,39,40] using a range of different methods. The gene discussed is CDH1; the disease is neoplasm.