However, further observations that mice deficient in IL-12p35 subunit [35,36] or IL-12Rβ2 chain [37] or IFN-γ [38] were susceptible to EAE together with data showing that the administration of IL-12 during the early phases the disease suppressed EAE in an IFN-γ-dependent manner [35], undermined the paradigm that Th1 cells were the main pathogenic cell subset in EAE and MS. Here, IFNG is linked to myeloid sarcoma.