The present results shown here suggest that cardiomyocyte‐derived ACh plays a pivotal role in modulating myocardial energy metabolism, for example, activated myocardial glucose utilization, and angiogenesis in ischemic areas after MI and that overexpression of cardiomyocyte ChAT improves survival after MI through antiremodeling effects or ischemia–reperfusion injury. This evidence concerns the gene CHAT and myocardial infarction.