Dravet syndrome, an epileptic encephalopathy affecting children, largely results from heterozygous loss-of-function mutations in the brain voltage-gated sodium channel gene SCN1A. Heterozygous Scn1a knockout (Scn1a+/−) mice recapitulate the severe epilepsy phenotype of Dravet syndrome and are an accepted animal model. This evidence concerns the gene SCN1A and Dravet syndrome.