A potential role of CaMKII signaling in cell survival is supported by the fact that CaMKIIα knock-out (Camk2a−/−) mice display increased vulnerability to ischemic injury after tMCAO and photothrombotic stroke, as evidenced by increased cortical infarct sizes compared to wildtype (Camk2a+/+) littermates [25,133]. Here, CAMK2A is linked to stroke disorder.