Given that seven of the females in this study with CIS or MS had IgM antibody responses to EBV, and EBV latent infection can upregulate BAFF secretion in infected B cells (75), it is tempting to speculate that EBV reactivation could be the trigger for increased serum BAFF and lower expression of CD32b on some B cell subsets in people at the earliest stages of MS. The gene discussed is TNFSF13B; the disease is disease arising from reactivation of latent virus.