Moreover, host gene expression analysis revealed activation of pathways linked to hypercytokinemia and interferon signaling in MS-derived SLCLs and an upregulation of the transcription factor forkhead box protein 1 (FOXP1), which is important for maintaining EBV lytic gene expression, altogether indicating that a population of EBV-positive B cells, which fail to control EBV latency, may contribute to MS pathogenesis by driving B- and T-cell inflammation, particularly during active disease (111). Here, FOXP1 is linked to myeloid sarcoma.