Deletion or deregulation of E‐cad is also correlated with the infiltrative and metastatic ability of the tumour because of disruption of the cadherin‐catenin complex, with consequent loss of cell adhesion and concomitant increase in cell motility.4, 5 In gastric carcinoma in particular, defective mechanisms of E‐cad are well associated with cancer metastatization; patients carrying any somatic E‐cad alterations show the worst prognosis and shortest probability of overall survival (OS).6 This evidence concerns the gene CDH1 and neoplasm.