Background: Recently, many studies have indicated the potential roles of vitamin D in rheumatoid arthritis (RA). In the present study, the published available GWAS summary data was used to perform two-sample Mendelian randomization (MR) to infer the causal effect between circulating vitamin D levels and RA risk.Methods: Single nucleotide polymorphisms (SNPs) which significantly associated with exposure were selected as instrumental variables from larger-scale genome-wide association study (GWAS). The robust analytical methods including MR Egger, inverse variance weighted (IVW), weighted median and weighted mode were conducted to infer the causal links. Results: The IVW method suggested that there was no causal relationship of genetically predicted circulating vitamin D on RA (Asian: odds ratio (OR)=0.911, 95% confidence interval (CI), 0.542-1.534, P=0.727; European: OR=0.897, 95% CI, 0.633-1.269, P=0.538). MR Egger (Asian: OR=0.937, 95% CI, 0.373-2.352, P=0.895; European: OR=0.853, 95% CI, 0.469-1.553, P=0.639), weighted median (Asian: OR=0.895, 95% CI, 0.499-1.606, P=0.711; European: OR=0.885, 95% CI, 0.620-1.264, P=0.503) and weighted mode (Asian: OR=0.904, 95% CI, 0.515-1.588, P=0.738; European: OR=0.898, 95% CI, 0.618-1.306, P=0.604) demonstrated that vitamin D was not directly related to RA as well. Conclusions: The MR analysis indicates that there is no evidence of causal effect of genetically predicted circulating vitamin D levels on RA risk.