DS has been successfully recapitulated in well-characterized mouse models using several genetic strategies, including heterozygous Scn1a+/− models, the R1407X knock-in model resulting in a truncated α-subunit, and others.11,12,24 Importantly, the Scn1a+/− model recapitulates seizure-modifying efficacy for several treatments clinically indicated for DS patients. The gene discussed is SCN1A; the disease is Dravet syndrome.