Mice with heterozygous deletion of Scn1a that reduced sodium currents in GABAergic inhibitory interneurons recapitulated many of the clinical features observed in patients with Dravet syndrome (Yu et al., 2006; Tai et al., 2014), suggesting that the functional impairment of inhibitory interneurons were likely to cause the epilepsy phenotype. Here, SCN1A is linked to Dravet syndrome.