Exploration of NaV1.1 biophysics and neuronal dysfunction has provided inroads into the pathophysiology of SCN1A channelopathies by revealing deficits of excitability across several interneuron populations, a correlation between profound loss-of-function and the more severe phenotype of DS, and an interesting divergence between NaV1.1 gain-of-function and the distinct clinical syndromes of EIDEE and FHM3. This evidence concerns the gene SCN1A and Dravet syndrome.