The causal, major-effect, SCN1A variant may need to act against a broadly compromised genomic background to generate the full Dravet syndrome phenotype, whilst genomic resilience may help to ameliorate the risk of premature mortality in adult Dravet syndrome survivors. The gene discussed is SCN1A; the disease is encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.