This capacity of modulate the IFN-β activity and its accessibility in serum makes sIFNAR2 an attractive target molecule to be considered in MS, due to the key role of endogenous IFN-β in the pathophysiology of MS and even more if we consider the use of exogenous IFN-β as a treatment. The gene discussed is IFNB1; the disease is myeloid sarcoma.