Despite MS/EAE being traditionally perceived as mainly IFNγ-mediated, deletion of a negative regulator of IFN-α /β, c, in myeloid cells of EAE mice, resulted in uncontrolled type I IFN signaling and white matter microglia activation due to prolonged STAT1 phosphorylation, leading to disease exacerbation (78). The gene discussed is IFNG; the disease is myeloid sarcoma.