2016; Xu et al. 2016; Tsushima et al. 2017; Xia et al. 2017), and this serine residue is phosphorylated by cyclin‐dependent kinase 1 (CDK1)/cyclin B (Taguchi et al. 2007), protein kinase C delta (Qi et al. 2011), extracellular regulated kinase (ERK) (Prieto et al. 2016), and Ca2+/calmodulin‐dependent kinase II (CaMKII) (Xu et al. 2016). CaMKII is activated in the noninfarct area after MI (Singh et al. 2012), and the level of oxidized CaMKII, an activated form of CaMKII, has been reported to be increased in the diabetic myocardium (Luo et al. 2013). This evidence concerns the gene PRKCD and myocardial infarction.