It has been reported that adenoviral overexpression of ZFP36 results in protection against bone loss and reduced inflammatory cell infiltration in experimental periodontitis in rats (56). Consistent with these findings, ZFP36-delta ARE mice, in which the stability of ZFP36 mRNA is enhanced by the deletion of a 136-base instability motif in the 3’ UTR of ZFP36 mRNA, show the increased levels of ZFP36 expression in tissues (57) and are protected from anti-type II collagen antibody-induced arthritis, imiquimod-induced dermatitis, and experimental autoimmune encephalomyelitis (57). This evidence concerns the gene ZFP36 and experimental autoimmune encephalomyelitis.