Heterozygous (Scn1a+/−) mice had spontaneous seizures and occasional deaths beginning on postnatal day 21, attributed to haploinsufficiency of Nav1.1 channels, and homozygous Scn1a knockout (Scn1a−/−) mice developed severe ataxia and seizures and died on postnatal day 15, corresponding to the LOF effect (59). The gene discussed is SCN1A; the disease is cerebellar ataxia.