Mutations in ATP1A1, ATP1A2, or ATP1A3 cause severe neurological disorders, such as Charcot-Marie-Tooth disease, complex spastic paraplegia, familial hemiplegic migraine type 2, rapid-onset dystonia-parkinsonism, alternating hemiplegia of childhood, or cerebellar ataxia, areflexia, pes cavus, optic atrophy, and sensorineural hearing loss (CAPOS) syndrome [42,43,44,45]. This evidence concerns the gene ATP1A2 and hereditary optic atrophy.