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. The gene discussed is SCN1A; the disease is Epileptic encephalopathy.