Although the primary causes of the human ATP1A2- and ATP1A3-related neurologic disorders described above are missense mutations, these heterozygous knockout (deletion) mice have been shown to exhibit the phenotypes of FHM2 (Atp1a2+/-) [42] and RDP but not AHC (Atp1a3+/-) [43,44]. The gene discussed is ATP1A2; the disease is nervous system disorder.