These HERV-W/MSRV Env pro-inflammatory properties have been attributed to the protein’s ability to trigger the Toll-Like Receptor 4 (TLR4) [126,128,129], leading to the overexpression of the same proinflammatory cytokines involved in MS, such as interleukins 1 and 6 (IL-1, IL-6) and Tumor Necrosis Factor α (TNF-α), and inducing lymphocyte Th-1 polarization [127,128,130]. The gene discussed is ERVW-1; the disease is myeloid sarcoma.