Given this multifactorial interplay, involving genetic predisposition and exogenous agents (Christensen, 2005; Ryan, 2011), the HERV-W/MSRV Env superAg activity is the most probable HERV-derived contributor to MS clinical manifestations, inducing inflammatory effects coincident with the major hallmarks of MS (van Horssen et al., 2016). The gene discussed is ERVW-1; the disease is myeloid sarcoma.