This suggests that the postulated superior efficacy of NAT at least in some individuals as described by studies on observational cohorts (27, 28) might be rather due to a superior control of non-T-cell invasion than control of T-cell transmigration itself, thus further underlining the increasingly appreciated role of non-T cells in MS pathophysiology (29–31). The gene discussed is BRD2; the disease is myeloid sarcoma.