SCN1A and Dravet syndrome: Functional consequences of FHM3‐related SCN1A mutations in transfected cells indicate an overall gain of function of NaV1.1 channels.4, 5, 6 This sharply contrasts with the loss of function observed with mutations causing Dravet syndrome, resulting in loss of NaV1.1 expression predominantly affecting GABAergic interneurons.7, 12, 13, 14 In mice, this loss of function results in spontaneous seizures and large‐amplitude interictal spikes, which we did not observe in Scn1aL263V mice.