Given previous reports linking TLR’s and the GABAB receptor subtype with neuroinflammation, particularly with relevance to MS pathogenesis, we sought to explore the impact of baclofen (the GABAB receptor agonist) on TLR3 and TLR4-induced inflammatory signaling both centrally and in the periphery, using murine glial cells and human peripheral blood mononuclear cells (PBMCs) isolated from healthy individuals and newly-diagnosed patients with the relapsing-remitting (RR) form of MS patients. The gene discussed is TLR4; the disease is myeloid sarcoma.