To test this hypothesis, we generated Nhe1 heterozygous Apoe–/–Nhe1+/– mice and their littermate Apoe–/–Nhe1+/+ control mice, because Nhe1 homozygous-deficient mice develop ataxia and epileptic-like seizures, show postnatal growth arrest, and often die within a month after birth16,17. The gene discussed is SLC9A1; the disease is cerebellar ataxia.