This is consistent with our data showing an absence of IgA+ B cells in the CSF of MS subjects who did not have active disease at the time of the CSF collection, and leaves open the possibility that egress of IgA-producing plasmablasts from the gut that are capable of immunomodulation in the CNS occurs during an inflammatory relapse, as proposed by Rojas and colleagues (67). The gene discussed is CD79A; the disease is myeloid sarcoma.