Western blot analyses revealed that treatment with VPA induced PARP cleavage and activation of caspase-3 evidenced by the increase of cleaved caspase-3 in the HPAF-II and MPanc96 cells dramatically (Fig. 1e and g), but only marginally promoted apoptosis in MiaPaca-2 and Panc-1 (data not shown), suggesting that VPA selectively induced caspase-dependent apoptosis in the EGFR/ErbB2/ErbB3-coexpressing pancreatic cancer cells. The gene discussed is CASP3; the disease is pancreatic neoplasm.