CAMK2G and ischemic stroke: Overall, in ischemic stroke, there is compelling evidence supporting rapid CaMKII activation immediately after I/R insults, and activated CaMKII plays a crucial role in mediating excitotoxicity-induced neuronal death through necrotic, apoptotic, and possibly autophagic pathways and contributes to secondary oxidative damage, neuroinflammation, and BBB dysfunction, indicating that inhibition of CaMKII may be a promising therapeutic strategy to limit brain damage in acute phase of ischemic injury.