In the present study, we first showed that fingolimod restores the BBB dysfunction induced by sera from MS patients; specifically, pretreatment with fingolimod-phosphate restored the decreased expression levels of claudin-5 protein/mRNA and TEER values in the BMECs following exposure to sera derived from RRMS and SPMS patients, thus suggesting that fingolimod-phosphate is able to restore BBB damage and make the BBB less permeable in both the relapse and progressive stages of MS. This evidence concerns the gene CLDN5 and myeloid sarcoma.