SCN1A (34–36); however, limited success in the treatment of Dravet syndrome persisted (34, 37) in part due to the lack of understanding that inhibitory interneurons and not pyramidal neurons had altered excitability as a result of LOF SCN1A mutations (15, 16). Here, SCN1A is linked to encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.