In support of this, a recent study showed that reactivation of Scn1a expression in a Scn1a conditional knock-in mouse model can rescue seizure activity and behavioral abnormalities, and normalize interneuron excitability, even months after symptom onset.61 Together, these data suggest that disease phenotype may be reversed and strongly support continued development of AAV9-REGABA-eTFSCN1A as a novel gene therapy with the potential to durably rescue multiple phenotypes in DS patients. The gene discussed is SCN1A; the disease is Dravet syndrome.