After the establishment of HF (4 weeks after myocardial infarction; MI), a subsequent six-week treatment with βIIV5-3 abolished the increased cardiac PKCβII translocation and activity (Fig. 3A), but not the activity of α, βI, δ, γ and PKCε (Fig. S2), and diminished the co-immunoprecipitation of PKCβII and the 20S proteasome as well as its phosphorylation (Fig. 3B). This evidence concerns the gene PRKCE and myocardial infarction.