Since NaV1.1 is primarily expressed within inhibitory interneurons and many epilepsy-associated SCN1A variants were found to predispose to a loss of channel function, the pathophysiology of SCN1A disorders has been conceptualized as driven by an interneuronopathy that predisposes to cortical hyper-excitability through disinhibition (2, 3). Here, SCN1A is linked to epilepsy.