Taken together, our data suggest that EBNA2 and RBPJ tend to bind to MS-related intervals more than expected by chance; EBNA2 distribution across the genome overlaps with VDR occupancy in B cell lines, suggesting that non-heritable risk factors influence each other and interact with MS susceptibility loci in pathogenically relevant immune cell subsets [43, 44]. The gene discussed is RBPJ; the disease is myeloid sarcoma.