Given that GRK2 can block the pro-contractile and other beneficial signaling of cardiac β2AR in HF, and also that its action on β2AR induces recruitment of βarrs with all their aforementioned myriad effects on this receptor’s signaling, we hypothesized, in the present study, that cardiac GRK2 blockade in vivo might enhance β2AR signaling post-MI. Here, ADRB2 is linked to myocardial infarction.