NFKB1 and neuromyelitis optica: Binding of NMO-IgG to AQP4 triggers numerous immune-associated pathways, including interferon, chemokine/cytokine, complement, and NF-κB signaling pathways, which can result in the recruitment of innate immune cells into the CNS, and the concomitant amplification and exacerbation of tissue dyshomeostasis and injury (4–6).