A better knowledge of the interactome of GRK2 and its modulation in the different cardiac cell types, of the molecular mechanisms and stimuli leading to increased GRK2 expression in settings of cardiac hypertrophy, ischemia/reperfusion, and post-infarction remodeling, and of the detailed temporal pattern of such changes would help to fine-tune the therapeutic strategies targeting this protein. This evidence concerns the gene GRK2 and infarction.