The accumulation of ex vivo BTK+CXCR3+ B cells in the blood of clinical NTZ responders as well as the impairment of in vitro CXCR3+ memory B cell migration across the blood-brain barrier and the maturation of these cells into ASCs by evobrutinib further highlight the potential of BTK as a therapeutic target in MS. This evidence concerns the gene BTK and myeloid sarcoma.