ACSL4 and epilepsy: The pathological process of epilepsy is also deeply intertwined with ferroptosis; iron overload in epileptic foci promotes the generation of lipid peroxides through ACSL4-mediated arachidonic acid metabolism, while decreased GPX4 activity further weakens antioxidant defenses, forming a vicious cycle of “neuronal hyperexcitability-oxidative stress.” Preclinical studies show that using Liproxstatin-1 to inhibit ferroptosis can significantly reduce the frequency of seizures and protect hippocampal neurons (Batista et al., 2021).