Oxidative stress is observed in HF, after myocardial infarction (MI) and with increased levels of Ang‐II.100 Moreover levels of CaMKIIδC are also increased during pressure overload, HF and sustained β1‐AR stimulation thus both factors contributing in outcomes of adverse cardiac events.101, 102, 103 Hence, CaMKII Inhibition appears to be cardio‐protective after MI by reducing apoptosis and remodelling associated with excessive stimulation of β‐AR signalling and Ang‐II.100, 104. Here, CAMK2G is linked to myocardial infarction.