Such high morbidity6 also indicates the need to consider patient-specific aspects of oral tumor biology; variable tumor composition is due in part to regional differences in niche properties and cell signaling that can lead to cells undergoing epithelial-to-mesenchymal transition (EMT),7 which is the process where cells lose expression of epithelial (E-Cadherin) but gain mesenchymal markers (N-Cadherin). This evidence concerns the gene CDH2 and neoplasm.