Similar to the effect of PKCβII inhibition in the myocardial infarction-induced HF model in rats, sustained treatment with βIIV5-3 (but not the βI inhibitor) between weeks 11–17, reduced PKCβII activity to basal levels (Fig. 5A), restored ATP-dependent proteasomal activity and decreased the levels of misfolded cardiac proteins to those seen in control animals (Fig. 5B–D). This evidence concerns the gene CACNA1A and myocardial infarction.