In contrast, the second group of studies reported a fast (3 min) and prolonged (at least 30 min) increase in CaMKII phosphorylation of T286 in the total homogenate and membrane fractions (including PSD/synaptosomal) during ischemia [11], which stayed elevated for at least 30–60 min or longer during the reperfusion [22,23,24]. This evidence concerns the gene CAMK2G and ischemia.