Arid5a can stabilize OX40, STAT3, and T-bet mRNAs in T cells to promote Th17- and Th1-dependent pathology in mouse models of EAE.196–198 However, Arid5a is shown to be induced by IL-6 in RA patients with the potential function to attenuate Th17 cell differentiation through physically interacting with RORγt.199 Mechanisms underlying this discrepancy and the detailed role of Arid5a in competition or cooperation with other RBPs in the development of Th17-dependent autoimmunity remain to be identified. This evidence concerns the gene STAT3 and Autoimmunity.