In C57BL/6 mice subjected to an experimental autoimmune encephalomyelitis model, one of the most common animal models to study MS, TRPV1 channels lead to an increase in calcium influx, augmenting ATP secretion, and then activating NLRP3 inflammasome and aggravating clinical outcomes of experimental autoimmune encephalomyelitis, which suggests that the ATP signaling pathway may be engaged in MS – microglia – EBV route (Zhang et al., 2021b). The gene discussed is NLRP3; the disease is experimental autoimmune encephalomyelitis.