Moreover, in our experimental setting, the greater effect of the fluvastatin/gemcitabine combination could also be dependent on a higher concentration and prolonged half-life of the active mono-, di- and triphosphate metabolites of gemcitabine inside the pancreatic tumour cells due to the fluvastatin induction of the expression of dCK, which activates the drug by phosphorylation, and the reduction of 5′-NT, which removes the phosphate group from cytotoxic metabolites (Danesi et al, 2003). Here, DCK is linked to pancreatic neoplasm.