The COX-2-dependent upregulation of Snail in inflammatory conditions reduces E-cadherin and contributes to EMT. Its higher cytoplasmic expression in epithelial cells may be due to the protein E-cadherin's increased production rate and lack of mobility or adherence to cell membranes [24]. At the front of cancer cells, the E-cadherin-mediated cell-cell adhesion system is deactivated due to tyrosine phosphorylation of Beta-catenin [25]. Here, SNAI1 is linked to cancer.