Some studies using in vivo or in vitro models indicate that GSK‐3β may regulate neuronal apoptosis through activation of NF‐κB, β‐catenin or CREB signalling pathways.28, 29, 30 Other studies report that GSK‐3β can activate Nrf2 signalling to attenuate β‐amyloid‐induced oxidative stress in Alzheimer's disease models.31, 32 Therefore, the role of GSK‐3β and its downstream pathways in hydrogen treatment against TBI should be fully investigated in the future. This evidence concerns the gene CREB1 and early-onset autosomal dominant Alzheimer disease.