Moreover, increased extracellular oxidation enhances the potency of AMPAR‐induced active responses, specifically tension currents, at low concentrations.[59] These observations help elucidate why the application of endogenous intracellular antioxidants such as glutathione is ineffective in patients with epilepsy.[60] Prdx6 inhibition of aiPLA2 activity may represent a promising therapeutic strategy to mitigate neuronal oxidative stress and reduce seizures in patients with clinically refractory metabolic hydroxyglutarate epilepsy caused by D2HGDH deficiency. The gene discussed is PRDX6; the disease is hyperinsulinemic hypoglycemia, familial, 4.