This poses an important therapeutic challenge because, although being both recognized as autoimmune diseases, they show opposite therapeutic responses to DMARDs, with the TNF-inhibitors used for RA that are known to exacerbate the course of MS or provoke demyelination [17,18], while IFN-beta used for MS has a controversial role in RA pathogenesis and has been suggested to be capable of provoking some cases of iatrogenic RA [19,20]. This evidence concerns the gene TNF and rheumatoid arthritis.