Furthermore, only the targeted TAU ablation on excitatory neurons improved survival, reduced network hyperexcitability, and ameliorated some social and behavioral abnormalities in a DS mouse model, in line with previous reports.5 Next, the authors examined the PI3K-AKT-mTOR pathway, an overactivated pathway in epilepsy syndromes and an attractive therapeutic target. The gene discussed is AKT1; the disease is epilepsy syndrome.