For example, protein truncating variants in SCN1A are more likely than missense variants to cause Dravet syndrome rather than milder epilepsies [28], and the electrophysiological consequences of particular SCN2A variants might predict age of onset and treatment response [4]. The gene discussed is SCN2A; the disease is encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.