SCN1A and Dravet syndrome: Over 85% of DS cases are caused by heterozygous loss-of-function variants in a single copy of the SCN1A gene, encoding the alpha subunit of the voltage-gated type I sodium channel (NaV1.1).10 NaV1.1 is predominantly expressed within the axon initial segment of GABAergic inhibitory interneurons, where it generates and propagates action potentials.11 Genetic reduction of NaV1.1 substantially reduces the frequency and amplitude of action potentials generated by GABAergic inhibitory interneurons, thereby impairing their inhibitory function, which is dependent on high-frequency firing.12–14