In a whole mouse model lacking functional NADPH oxidase or with CaMKII inhibition, mice were highly resistant to sinus node dysfunction induced by angiotensin II infusion, suggesting that CaMKII plays an important role in this pathway (Swaminathan et al., 2011) and further demonstrating the therapeutic benefit of a targeted approach focused on ox-CaMKII in DM. Here, CAMK2G is linked to diabetes mellitus.