Compared to other positive inotropic strategies in heart failure therapy, the biochemical and phenotypic effects of RKIP substantiate the hypothesis that a successful positive inotropic strategy should not induce an unselective activation of βAR downstream targets (as for βAR agonists, PDEIII inhibitors or β1AR‐overexpressing mice) but rather circumvent activation of the RyR2 (as in PLN–/– mice, SERCA2a or βARKct overexpression) or even protect from RyR2 sensitization (as in GRK2–/– mice, S100A1 and RKIP transgenic mice) (Kairouz et al. This evidence concerns the gene ADRB1 and heart failure.