HK2 and Stroke: To mitigate the side effects, we could improve the strategies as follows: using nanocarriers or ligands (e.g., TSPO ligands) to deliver HK2 inhibitors preferentially to microglia/macrophages rather than neurons [46]; transient HK2 inhibition during acute inflammatory phases (e.g., post‐stroke) could limit chronic metabolic consequences [47]; coupling HK2 inhibition with antioxidants or metabolic supplements (e.g., lactate) might counteract neuronal energy deficits [48, 49].