VPA not only preferentially inhibits proliferation/survival of aforementioned subtype of pancreatic cancer cells in a dose-dependent manner (Fig. 1), but also potently induces caspase-dependent apoptosis in EGFR/ErbB2/ErbB3-coexpressing pancreatic cancer cells within its clinically achievable range [40~100 mg/L (0.24~0.6 mmol/L)] (Fig. 1). Here, EGFR is linked to familial pancreatic carcinoma.