Genome-wide expression profiling and functional experiments showed that IFN-β non-responders had increased expression of co-stimulatory molecule CD86 on myeloid DCs before initiation of IFN-β therapy, implying that the clinical response to IFN-β may be related to the activation status of myeloid DCs [60], which is needed to elucidate the exact mechanisms of the nexus between activation status of myeloid DCs and action of IFN-β in MS/EAE in the future. The gene discussed is IFNB1; the disease is myeloid sarcoma.