CAMK2G and ischemia: Furthermore, reports that CaMKII is susceptible to oxidation (ox-CaMKII(Met281/2)), promoting autonomous activation (Erickson et al., 2008; Palomeque et al., 2009), suggests the sub-cellular environment in ischemia (acidosis, high cellular Ca2+) and reperfusion (Ca2+ overload, oxidative stress) provides an optimal setting for rapid CaMKII activation – and highlights the potential for intervention strategies targeting CaMKII.