However, recent work in the myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) mouse model of MS-associated neuropathic pain has implicated an additional component involving activation of the complement system and the NLRP3 inflammasome in the lumbar dorsal root ganglia (DRGs) in the pathobiology of MS-associated neuropathic pain (Yousuf et al. 2019). This evidence concerns the gene MOG and experimental autoimmune encephalomyelitis.