Future research must aim to clarify isoform-specific functions of HDACs and HATs across different CNS cell types and ischemic stages, develop cell-targeted or brain-penetrant epigenetic modulators with minimal off-target effects, explore combinatorial therapies that leverage HDAC inhibitors with HAT activators or immune modulators, and investigate long-term epigenetic reprogramming effects on neuronal regeneration, glial scar formation, and post-stroke cognitive outcomes. This evidence concerns the gene HDAC9 and Stroke.