SCN1A and Dravet syndrome: Multiple lines of evidence have established impaired excitability of GABAergic inhibitory interneurons due to NaV1.1 haploinsufficiency as fundamental in driving key DS phenotypes, and suggest that enhancement of GABA signaling may improve seizure control and other manifestations associated with DS.12,13,15–21 On the contrary, pan-neuronal overexpression of Nav1.1 in both GABAergic inhibitory interneurons and excitatory neurons would lead to an opposing physiological effect, increasing the excitability of both cell types and further disrupting the balance of excitation and inhibition.50–53