Irrespective, our study did not support a causal effect of insulin and sulfonylureas on RA risk, but on the other hand suggest that whatever mechanism that drives the association between the genetic variation in the thiazolidinedione target and RA risk is not shared with any glucose-lowering drugs, or mediated via other mechanisms shared by the genetic variation in targets of these drugs. This evidence concerns the gene INS and rheumatoid arthritis.