A dual-vector approach using split-intein technology enabled interneuron-specific SCN1A gene replacement, providing strong protection against mortality and seizures in DS mouse models (i.e., Scn1afl/+;Meox2-Cre and Scn1a+/R613X) while avoiding the adverse effects observed with pan-neuronal expression [163]. The gene discussed is SCN1A; the disease is Dravet syndrome.