CAMK2G and ischemia: Proteolytic processing of CaMKII might thus represent a pathological mechanism downstream of ischemia-activated and Thr286 phosphorylated CaMKII, and the uncontrolled kinase activity of ∆CaMKII might contribute to the neurotoxic role of sustained CaMKII activity after ischemia by phosphorylating specific neuronal proteins to direct cell death.