In an effort to investigate the underlying mechanism, we found that while the expression of cyclin-dependent kinase (CDK) inhibitor P21, one of the most commonly induced genes by HDACi [29], was significantly induced in all four pancreatic cancer cell lines upon treatment with VPA; however, the protein levels of cyclin D1 were only significantly decreased in the EGFR/ErbB2/ErbB3-coexpressing HPAF-II and MPanc96 cells (Fig. 1d). This evidence concerns the gene CCND1 and familial pancreatic carcinoma.