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. This evidence concerns the gene D2HGDH and hyperinsulinemic hypoglycemia, familial, 4.