Of note, intrathecal B cells from treatment-naïve MS patients with clinically active disease, displayed an almost similar migratory phenotype as depicted by co-expression of CD27 and upregulation of CXCR4 and CXCR5 genes, thus strengthening the fundamental interplay between CSM memory phenotypes and the CXCL-12/-13 axis for B-cell penetration through the BCSFB. The gene discussed is CXCR5; the disease is myeloid sarcoma.