IFNG and myeloid sarcoma: The Th1-driven nature of the EAE/MS disease was challenged by the finding that IFNγ- and IFNγ-receptor-deficient mice, as well as mice that lack other molecules involved in Th1 differentiation, such as IL12p35, IL12 receptor β2 (IL12Rβ2), and IL18, were not protected from EAE, but instead were more susceptible to the disease [21–25].