Therefore, the balance between Th17 and Treg, as well as Th1/Th2, has long been considered as 1 of the important factors in the treatment of autoimmune diseases including RA.[42] Anti-TNF therapy may lead to the failure of the Treg suppression effect on cell proliferation to reduce Foxp3 mRNA expression.[43] ETN, as a kind of TNF-α inhibitors, is the first TNF-α inhibitor for the treatment of RA. This evidence concerns the gene TNF and autoimmune disease.