Dravet syndrome (DS) is a rare and severe form of epilepsy that causes intellectual disability and motor deficits and can lead to premature death. A loss-of-function mutation in one copy of SCN1A, encoding the voltage-gated sodium channel (NaV)1.1 α subunit, is the most frequent alteration found in DS patients and has been linked with inhibitory neuron dysfunction. Despite the potential of gene therapies, AAV-mediated SCN1A gene replacement for DS has not been possible yet due to AAV genome size constraints.