SCN1A and Dravet syndrome: Symptoms and mechanisms of DS have beenwell modeled and studied in mice,,, and more recently, in iPS-derived neural cells;, however, published data have shown controversial evidence regardingthe importance of Nav1.1 in inhibitory and excitatory neurons., When studying DS, it is important to take into consideration theelevated number of already described SCN1A mutations, as differentalterations can lead to slightly different outcomes. Cell reprogramming allows the generation of patient-specificneural cells that may recapitulate some disease mechanisms.