Interestingly, reduction in the expression of SCN8A has been shown to extend survival in Scn1a+/- haploinsufficient mouse models of DS and channelopathies involving Kcna1 and Kcnq2 [153,154,159], highlighting the broader therapeutic potential of addressing hyperexcitability through modulation of Nav1.6 expression. Here, SCN8A is linked to Dravet syndrome.