| Summary: | Abstract Pathogenic loss‐of‐function variants in SCN1B are linked to Dravet syndrome (DS). Previous work suggested that neuronal pathfinding defects underlie epileptogenesis and SUDEP in the Scn1b null mouse model of DS. We tested this hypothesis by inducing Scn1b deletion in adult mice that had developed normally. Epilepsy and SUDEP, which occur by postnatal day 21 in Scn1b null animals, were observed within 20 days of induced Scn1b deletion in adult mice, suggesting that epileptogenesis in SCN1B‐DS does not result from defective brain development. Thus, the developmental brain defects observed previously in Scn1b null mice may model other co‐morbidities of DS.
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