They have shown that IFN-β reduced the proliferative response to MBP and myelin and augmented the expression of the CTLA-4 intracellular molecules, thus suggesting that the rise in the CTLA-4 molecules in MS patients could lead to lymphocyte apoptosis and thus shed light on the potential mechanisms involved in the therapeutic response to IFN-β [87]. Here, IFNB1 is linked to myeloid sarcoma.