Emerging clinical evidence from patients with GABAB receptor encephalitis-associated epilepsy reveals significant elevation of cerebrospinal fluid ferroptosis biomarkers such as malondialdehyde (MDA) and 4-HNE, along with glutathione depletion and ACSL4 upregulation, mechanistically linked to exosomal miR-92a-3p-mediated NF2/P-YAP pathway suppression that worsens neuronal iron overload and lipid peroxidation (Zhang et al., 2025). Here, ACSL4 is linked to epilepsy.