The beneficial role of the eNOS-derived NO has been demonstrated also in congestive heart failure (HF) in the study by Jones et al. in which the authors, by using a mouse model of infarct-induced HF, showed that eNOS overexpression enhanced animal survival, inhibited pulmonary edema, and improved cardiac function but did not attenuate the cardiac hypertrophy or improve cardiac contractility [59]. This evidence concerns the gene NOS3 and cardiac hypertrophy.