A variety of engineered mouse models show RA-associated phenotypes and have been valuable in the investigation of causative mechanisms ranging from antigen-specific adaptive T cell responses (the K/BxN and TS1×HACII mice) to increased systemic cytokine levels [in tristetraprolin (TTP)−/− and gp130F759 mice]. This evidence concerns the gene ZFP36 and rheumatoid arthritis.