Our findings in the context of the above considerations, together with evidence for P2X7R in the development of experimental autoimmune encephalomyelitis [78] and microglia-oligodendrocyte crosstalk [79], propose a vicious cycle of Apo-SAA, IL-1β, and TLR2 leading to the demise of OPCs. The gene discussed is SAA2; the disease is experimental autoimmune encephalomyelitis.