Finally, given its key role as a critical regulator of innate and adaptive immunity (Table 2), loss of DUSP1/MKP-1 was also found to exacerbate a range of inflammatory phenotypes in mouse models including experimental colitis [40], anaphylaxis [41] and psoriasis [42], However, for reasons as yet unclear, loss of DUSP1/MKP-1 did not sensitize mice to the development of spontaneous age-dependent osteoarthritis, despite the involvement of an inflammatory process and mediators such as TNFα and interleukin-1β in this disease [43]. The gene discussed is DUSP1; the disease is age.