Currently, the clinical use of immunosuppressants and immunomodulatory drugs can mitigate the onset and progression of MS;[13] however, preventing and reversing the disease's progression remains challenging.[14] Thus, this study explores the role and mechanism of inflammatory factor CXCL13 in inducing BSCB structural and functional damage during EAE, in order to provide empirical evidence to elucidate the pathogenesis of MS and identify potential targets for prevention and treatment. This evidence concerns the gene CXCL13 and myeloid sarcoma.