Although there seems to be no study showing a direct correlation between the roles played by VRAC and CFTR in the RVD process of cardiomyocytes when ischemia-reperfusion injury occurs, during the phase of myocardial ischemia, intracellular ATP depletion prevents the activation of VRAC (Okada et al., 2019), and CFTR may provide myocardial protection in the event that VRAC activity is impaired, complementing the function of VRAC in regulating cardiomyocyte RVD. The gene discussed is CFTR; the disease is myocardial ischemia.