SCN1A and Dravet syndrome: Evidence of comparatively higher levels of Scn1a expression in GABAergic interneurons over pyramidal neurons, data from cell type selective Scn1a deletion studies, and demonstration of interneuron hypoexcitability have provided a framework for disinhibition as an underlying mechanism of DS, although age‐ and strain‐dependent increases in pyramidal neuron hyperexcitability have been reported.15