Researchers have shown that the persistent stimulation of G protein-coupled β-adrenergic receptors (β-ARs) can activate CaMKII and phosphorylate histone deacetylase (HDAC) in the cytoplasm and nucleus, which releases myocyte-specific enhancer factor 2 C (MEF2)-mediated inhibition of the expression of the hypertrophic gene atrial natriuretic peptide (ANP) and eventually leads to myocardial hypertrophy [19,20]. The gene discussed is NPPA; the disease is cardiac hypertrophy.