Indeed, we showed that the antiproliferative effect induced by vorinostat in CRC cells and in xenograft tumours was paralleled by downregulation of TS protein, the crucial enzyme for thymidilate synthesis and the target of 5-FU, and by upregulation of TP protein, a critical enzyme in the final step of the metabolic transformation of capecitabine to 5-FU. The gene discussed is TYMS; the disease is colorectal carcinoma.