Western blot analysis indicated that cleavage of CaMKIIα at site 2, leading to the formation of ΔCaMKIIα-long consisting of the intact kinase domain and the autoinhibitory/CaM-binding motif, occurred in both sham-operated and ischemic stroke mouse brains (Fig. 7, C–E), suggesting proteolytic processing as a physiological regulatory mechanism of CaMKII. The gene discussed is CAMK2A; the disease is ischemic stroke.