Epithelial–mesenchymal transition (EMT) is a transdifferentiation process, with the cells losing their polarity and contacts with neighbouring cells and subsequently acquiring mesenchymal-like and motile phenotypes.7 EMT plays pivotal and intricate roles in malignancy-related phenomena, including the cancer stem cell phenotype, drug resistance, circulating tumour cells and tumour-budding production.8,9 The loss of functional E-cadherin is considered as the hallmark of EMT.10 E-cadherin is negatively regulated by several transcriptional factors, including Snail, Slug, Twist and ZEB1/2.11,12. This evidence concerns the gene SNAI1 and neoplasm.