Dravet syndrome (DS) is a severe genetic epileptic encephalopathy with onset in infancy, often associated with drug‐resistant epilepsy, developmental slowing, cognitive impairment, occurrence of status epilepticus and elevated risk of early mortality.1, 2, 3 In most cases, the cause is a mutation in the voltage‐gated sodium channel type I alpha subunit gene, SCN1A. 4 The main challenges include seizure control, prevention of status epilepticus and optimizing development of cognitive function, where possible. Here, SCN1A is linked to status epilepticus.