CAMK2G and myocardial infarction: For instance, a β-arrestin-biased pepducin of the β2AR was recently shown to induce cardiomyocyte contractility and antiapoptotic signaling [50], whereas β-arrestin functioning as a scaffold for Ca2+/calmodulin-dependent protein kinase II (CaMKII) activity and exchange protein directly activated by cAMP (Epac) was detrimental to cardiac function following myocardial infarction [51, 52].