As we demonstrated before11, blocking protein–protein interaction between βIIPKC and its anchor protein (RACK1) with βIIV5-3 (the global inhibitor of βIIPKC15) improved isolated cardiomyocyte and whole heart contractility properties as well as cardiac remodeling in rats with myocardial infarction-induced heart failure (Fig. 1a–d; Supplementary Table 1). This evidence concerns the gene RACK1 and myocardial infarction.