The problem is that fluoropyrimidines are 80% metabolised to 5-fluoro-5,6-dihydrouracil (5-FUH2) by a key enzyme: dihydropyrimidine dehydrogenase (DPD). There is inter-individual variability in the activity of this enzyme, partly related to genetic factors [1]. An abundant literature has already shown that a decrease in the activity of this enzyme results in an increase in the half-life of 5-FU. Thus, patients with a deficit in DPD activity have a risk of overexposure to chemotherapy in this class, and consequently an increased risk of acute, early and severe toxicity.