CaMKII has been further shown to act as a molecular nexus linking neurohumoral stimulation to adverse cardiac remodeling and heart failure (HF) upon injury such as pressure overload, myocardial infarction and/or ischemia-reperfusion (IR; Maier and Bers, 2002; Zhang et al., 2003; Anderson et al., 2011; Erickson et al., 2013; Kreusser and Backs, 2014; Kreusser et al., 2014; Weinreuter et al., 2014; Capel and Terrar, 2015). Here, CAMK2G is linked to myocardial infarction.