It has been observed that IgA-secreting B cells that target gut microbes migrate from the gut to the CNS during inflammatory disease states, where they adopt a regulatory phenotype.17,18 By contrast, we previously found that proinflammatory T cells from patients with MS disproportionately express gut-homing receptors.19 Despite these recent advancements, the specific characteristics of the host-microbe interface at MS onset, as well as the effect of immunomodulatory disease-modifying therapies on this interaction, have yet to be closely examined. This evidence concerns the gene CD79A and myeloid sarcoma.