Since βarr2 also terminates the G protein-mediated signaling of the AT1R, stimulation of cardiac βarr2 activity and/or blockade of cardiac βarr1 activity at the AT1Rs of the heart might be sought after for the treatment of post-MI HF and the cardiac hypertrophy and adverse remodeling that accompany this devastating disease. This evidence concerns the gene AGTR1 and myocardial infarction.