TNF-α-mediated induction of IL-17 production by Th17 cells may play a role in the pathogenesis of RA, given that patients with active disease and high levels of TNF-α in the blood present increased levels of IL-17A in the joints and augmented frequency of peripheral and tissue-infiltrating pathogenic Th17 lymphocytes [43,44]. This evidence concerns the gene IL17A and rheumatoid arthritis.