IFNG and myeloid sarcoma: The Th1-driven nature of the MS disease was challenged by the discovery that IFN-γ and IFN-γ-receptor-deficient mice, as well as mice that lack other molecules involved in Th1 differentiation, such as IL-12p35, IL-12 receptor β2 (IL-12Rβ2, and IL-18, were not protected from EAE, but instead were more susceptible to the disease [32–36].