Although the precise mechanism underlying therapeutic effects of IFNβ on MS remains to be fully elucidated, previous studies proposed several possibilities, including the inhibition of Th1 cell development [6], induction of Th2 immune deviation [7], restoration of function of the disrupted blood-brain barrier [8], and downregulation of IFNγ-induced expression of class II major histocompatibility complex (MHC) molecules [9]. The gene discussed is IFNB1; the disease is myeloid sarcoma.