Objective：This study used mendelian randomization method to explore the relationship between telomere length and esophageal cancer，and to provide a theoretical basis for the prevention and treatment of esophageal cancer. Methods：Our study was based on previous esophageal cancer genome-wide association studies（GWAS）data（1 877 esophageal cancer patients and 2 084 controls），and nine telomere length-related single nucleotide polymorphisms（SNPs）reaching genome-wide association significant level were systematically selected as instrumental variables. Genetic risk score（GRS）and the inverse-variance weighting method（IVW）were applied to estimate the causal effect of telomere length on esophageal cancer risk. In addition，a stratified analysis based on age and gender was conducted to explore whether there was interaction between variables. Results：MR analyses indicated that both GRS and IVW methods suggested that there is no significant risk signal between genetically increased telomere length and esophageal cancer risk（GRS：OR=1.19，95%CI：0.81-1.77，P=0.380；IVW：OR=1.22，95%CI：0.81-1.84，P=0.380）. Subgroup analysis revealed significant heterogeneity between different gender. Conclusion：The study has not found a significant association between telomere length and the risk of esophageal cancer.