Dravet Syndrome (DS) is a severe epileptic encephalopathy associated with a high risk of premature death caused by sudden unexpected death in epilepsy (SUDEP). The disease is caused by haploinsufficiency of SCN1A gene, encoding the alpha subunit of the voltage-gated sodium channel Nav1.1. While DS onset is triggered by interneuron (IN) hypoexcitability, alterations in glutamatergic neurons contribute to its progression. Current gene therapy strategies aim to boost SCN1A gene expression in INs, prompting this study to investigate whether targeting them alone at various disease stages is sufficient to recover DS symptoms.A DS reversible mouse model (Scn1aStop/+) and the GABAergic Cre driver Gad2Cre were employed to constitutively abrogate Scn1a gene haploinsuffciency in INs. Scn1aStop/+;Gad2Cre mice were assessed for survival, susceptibility to spontaneous seizures through video-EEG recordings, and to febrile seizures through thermal induction.Results revealed that Scn1aStop/+;Gad2Cre mice were fully protected from SUDEP and febrile seizures, with a substantial reduction in spontaneous seizure frequency and severity. Intriguingly, while IN firing properties were normalized, Dravet mice exhibited reduced excitability of hippocampal pyramidal neurons at disease onset (P17-21), not recovered in Scn1aStop/+;Gad2Cre mice, suggesting a potential cell-autonomous defect. However, in the chronic stage (P48-70), their activity appeared normalized, likely by compensatory mechanisms. These findings highlight that restoring INs functionality before symptoms onset, mimicking a preventive therapy, allows to recover DS phenotype. To assess the effectiveness of IN-specific therapies administered after disease diagnosis, a better translational model will be established reactivating Scn1a expression in INs of adult mice using the inducible Gad2CreERT2 line.