Although the exact mechanism by which EBV plays a role in MS is unknown, a number of possible avenues have been suggested: cross-reactivity between EBV and MBP (i.e., molecular mimicry) [47,48]; increased production of alpha-B-crystallin due to EBV [49], a small heatshock protein that plays a role in regulating neuroinflammation [50]; and finally, antibody-dependent cell-mediated cytotoxicity [46]. The gene discussed is MBP; the disease is myeloid sarcoma.