Our findings suggested that OSBPL2 depletion potentiated H2O2-induced HEI-OC1 cell apoptosis by inhibiting the AKT/FOXG1 signaling pathway, implying therapeutic interventions targeting OSBPL2 and the AKT/FOXG1 pathway may be potential strategies for future treatment of AHL. This evidence concerns the gene FOXG1 and acute hemorrhagic leukoencephalitis.