MVP and pancreatic adenocarcinoma: Given that previous studies have associated aberrant methylation with an increased risk of PAAD development (24) and that promoter hypomethylation of oncogenes has been implicated as a promotive factor of tumorigenesis (25, 26), our observations suggest that the abnormal hypomethylation status of MVP may play a potential role in the initiation and progression of PAAD, which would result in gene overexpression, and activation of downstream signaling pathways.