Counteracting such dialog is therapeutically highly relevant, the more so as a central role of memory B cells in MS pathophysiology is supported by the fact that many disease-modifying drugs, including alemtuzumab, rituximab, fingolimod, and natalizumab, destroy or functionally deplete memory B-cell activity, while atacicept—an antagonist to B-cell-activating factor (BAFF) and A-proliferation-inducing ligand (APRIL) and or infliximab—an antagonist to TNF-alpha—which both stimulate memory B cells, were shown to worsen the disease (45). This evidence concerns the gene TNFSF13 and myeloid sarcoma.