Similarly, a lack of intrathecal IgG synthesis has been observed in the vast majority of patients with AQP4-IgG-positive NMOSD [15, 90, 91], in LGI1-IgG-associated encephalitis [92, 93], and in IgLON5-IgG-positive encephalomyelitis [92]), in a subset of patients with other CNS disorders of supposed autoimmune etiology such as Balo’s concentric sclerosis [17], Schilder’s disease [18], histopathologically defined “pattern II” and “pattern III” MS [16]. This evidence concerns the gene AQP4 and glycogen storage disease VI.