Heart failure (HF) is a condition in which the heart cannot supply the body's tissues with sufficient blood, resulting in a cascade of changes that lead to severe fatigue, breathlessness, and death.1 Hyperactivation of the renin‐angiotensin‐aldosterone system (RAAS) is known to occur in HF and is thought to trigger cardiomyocyte apoptosis, which is mediated by angiotensin II (Ang II).2,3 In clinics and hospitals, various strategies have been used to counteract the action of Ang II with limited success.4 This evidence concerns the gene AGT and hydrops fetalis.