Thus, the child with a de novo Y264H mutation described by Brown et al. [10] demonstrated recurrent hemichorea requiring treatment with haloperidol (Table S2), and in a second case reported by the same authors, a child with a maternally inherited F507L mutation, the phenotype was exclusively neurological, consistent with neuromyelitis optica and positive for AQP4 autoantibodies (a phenomenon recognized in the context of enhanced type I interferon signaling [22]). Here, AQP4 is linked to neuromyelitis optica.