In a large international cohort (~1000+ SCN1A mutation carriers), missense variants in conserved or functionally critical regions are strongly associated with classic DS (earlier onset, severe febrile seizures, more frequent status epilepticus), whereas variants in less conserved regions or truncating mutations at certain gene ends may be more often linked with milder phenotypes (e.g., GEFS+) [7]. Here, SCN1A is linked to Dravet syndrome.