G protein-coupled receptor kinase 4 (GRK4) aggravates cardiomyocyte injury during myocardial infarction (MI) by inhibiting histone deacetylase 4 (HDAC4)-mediated Beclin-1 transcription, while MI-induced cardiac dysfunction and remodeling are improved by deleting cardiomyocyte-specific GRK4 (30). This evidence concerns the gene BECN1 and myocardial infarction.