B cells from MS patients are deficient in their capacity to produce IL-10 after either TLR9 or CD40 stimulation, whereas TLR4-mediated IL-10 production was restored to normal levels in MS and further increased at relapse in the presence of CD40 signaling, thus, demonstrating that regulation of TLR4 and CD40 signaling in B cells may be a promising novel approach for MS therapy [47]. The gene discussed is TLR4; the disease is myeloid sarcoma.