It is conceivable that the genetic complexity of MS [including 200 autosomal variants outside the MHC locus, one on the X chromosome and 32 MHC alleles affecting MS risk (8)] might reflect the numerous pathways that EBV, a very complex virus with nearly 100 genes encoded by its genome (11), can exploit to alter the virus-host immune system balance and manifest its pathogenicity. Here, HLA-C is linked to myeloid sarcoma.