Beyond, it has been shown that S1Pr expression levels dynamically change during the formation of inflammatory lesion in MS, such as increased S1Pr1 and S1Pr3 expression levels on reactive astrocytes in active and chronic inactive MS lesions [104], indicating that astrocytes may act as target of fingolimod and siponimod within the CNS. This evidence concerns the gene S1PR1 and myeloid sarcoma.