Other studies in animal models of human diseases (allergic asthma, experimental autoimmune encephalomyelitis) have shown that the abatement of the Kv1.3 channel currents in vivo (by knocking out the channel or by treatment with ShK derivatives) ameliorates the progression of the disease and decreases the production of the effector cytokines IFN-γ, IL-4, IL-5 and IL-17, but enhances that of the anti-inflammatory cytokine IL-10 [60, 61]. The gene discussed is IFNG; the disease is experimental autoimmune encephalomyelitis.