IFNγ producing Th1 cells and IL-17 producing Th17 cells are highly encephalitogenic in the EAE model of MS, although they have distinct signature cytokine profiles, prompting us to hypothesize that molecules other than the signature cytokines regulate the effector function and contribute to the encephalitogenicity of both myelin-specific Th1 and Th17 cells. The gene discussed is IFNG; the disease is myeloid sarcoma.