TSC establishes a mechanistic link between genetic mutations and the complex clinical phenotype of intractable epilepsy.[7, 8] A key pathological feature of epileptogenesis in TSC is impaired potassium ion dynamics.[29, 30] While giant cells in TSC cannot generate action potentials, they may buffer potassium accumulation, potentially modulating neuronal excitability.[11, 17, 30] In this study, The outward current in the siNEAT1 group was stronger than in the other two model groups, and the addition of the mTOR inhibitor did not alter the outward potassium current. The gene discussed is MTOR; the disease is tuberous sclerosis.