As demonstrated in our ischemia–reperfusion study ex vivo, the prolonged interval from ischemia to ventricular beating arrest in the ChAT‐tg hearts supports the concept that ACh from the ChAT‐tg cardiomyocytes efficiently suppresses energy expenditure, leading to faster recovery of ventricular beating and salvage of the heart from the injury. The gene discussed is CHAT; the disease is ischemia.