IL-17-induced experimental autoimmune encephalomyelitis (EAE) was attenuated in mice with impaired p38-MAPK signaling, EAE was aggravated by increased IL-17 activity in the appellative experimental condition in mice lacking the p38-MAPK inhibitor MKP1 (Dusp1).56 These are reflective of the significance of IL-17 in the MAPK pathway. The gene discussed is DUSP1; the disease is experimental autoimmune encephalomyelitis.