Most genetic variants associated with RA risk have relatively modest effects on gene expression in a restricted number of cell types: an RA-associated variant in TRAF1 is associated with approximately 2-fold lower expression of TRAF1 in CD8 T cells and macrophages, with consequent higher production of pro-inflammatory cytokines including TNF and interleukin (IL)-6 [7]; a polymorphism in the IL-6 promoter, that has been associated with juvenile idiopathic arthritis, is an expression quantitative trait locus (eQTL) for IL-6 in synovial fibroblasts but not CD14+ monocytes [8]. This evidence concerns the gene TRAF1 and juvenile idiopathic arthritis.