To test the hypothesis that phosphorylation of TTP favours joint inflammation, we employed Zfp36aa/aa mice.15 Initially, responses were tested in the zymosan-induced air pouch inflammation model, which recapitulates aspects of the localised synovial inflammation observed in RA.32 Injection of zymosan into air pouches of Zfp36+/+ mice rapidly elevated levels of CXCL1 (chemokine (C-X-C motif) ligand 1), CXCL2, interleukin (IL)-6 and TNF in the exudate fluid. The gene discussed is ZFP36; the disease is inflammatory response.