Nevertheless, there is growing evidence of complement system activation in neuroinflammatory and neurodegenerative diseases, including brain traumatic injury (38, 39), amyotrophic lateral sclerosis (40, 41), multiple sclerosis (MS, 42, 43), antibody-mediated autoimmune encephalitidies such as MOG antibody (MOGAD) and GAD associated diseases, i.e., neurological disorders associated with anti-glutamic acid decarboxylase autoantibodies such as stiff-person syndrome, cerebellar ataxia and temporal lobe epilepsy (44–46). The gene discussed is MOG; the disease is aceruloplasminemia.