Clinical and basic researchers have reported various mechanisms involved in 5-Fu resistance including dysregulated expression of genes participating in fluorouracil metabolism such as dihydropyrimidine dehydrogenase and thymidylate synthase,24 acquired mesenchymal transformation or stem-like characteristics,25 and activation of intracellular signalling pathways including EGFR/Akt.12, 26 We reported here that treatment of ESCC cells with 5-Fu leads to elevated phospholevel of Erk and Akt. This evidence concerns the gene TYMS and esophageal squamous cell carcinoma.