Homozygous Scn1a−/− mice had seizures and ataxia, leading to death by day 15, while heterozygous Scn1a+/− mice showed spontaneous seizures, but some survived past 15 weeks.7 Whole-cell sodium current recordings from mouse neurons suggest that DS-causing mutations do not affect sodium currents in excitatory pyramidal cells, a finding that may be explained by upregulation of other sodium channels, such as Nav1.3. This evidence concerns the gene SCN1A and Dravet syndrome.