While this rise in GRK2 levels could function as a protective mechanism, aiming to safeguard the heart against potential cardiac toxicity induced by excessive catecholamines, an animal study demonstrated that cardiac-specific overexpression of GRK2, mirroring the upregulation levels seen in human heart failure (i.e., a 3-fold to 4-fold increase), significantly diminished β1-ARs’ signaling and cardiac contractile reserve [53]. This evidence concerns the gene GRK2 and heart failure.