Taken together, experimental evidence from human MS patients and experimental animal studies have led to a proposed mechanism in which an unknown trigger results in the aberrant activation of autoreactive CD4+ T cells in the immune periphery, after which these encephalitogenic CD4+ T cells enter the CNS from the choroid plexus (CP), are reactivated by local APCs in the CNS, and initiate a proinflammatory cascade that results in increased permeability of the blood-brain barrier (BBB), subsequent recruitment of proinflammatory immune cells, and subpial cortical damage (40). The gene discussed is CD4; the disease is myeloid sarcoma.