In addition, the data collectively support the role of IL-6 and IL-1β in RA as downstream mediators of TNFα for the induction of Th17 cell differentiation and are in an agreement with the results of reported clinical studies involving direct targeting IL-6 receptor or IL-1β in RA patients [39–42].  Alzabin et al. reported that an incomplete response of inflammation arthritis to anti-TNFα is associated with Th17 pathway [35]. This evidence concerns the gene TNF and rheumatoid arthritis.