Intriguingly, promoting histone acetylation via administration of the histone deacetylase (HDAC) inhibitor valproic acid has been shown to decrease neuronal apoptosis, neuroinflammation, and brain lesion size while improving neural plasticity and resulting in faster neurocognitive and neurologic recovery in pre-clinical models of traumatic brain injury, HS, and polytrauma (Nikolian et al., 2017, 2018; Chang et al., 2019). This evidence concerns the gene HDAC9 and brain injury.