Angiotensin‐converting enzyme inhibitor (ACEI) can act directly on myocardial tissue through inhibition of angiotensin II (Ang II) formation, which improves myocardial hypertrophy and fibrosis,1 reducing the overall morbidity and mortality of acute myocardial infarction (MI).2 However, the protective effects of ACEI may not be beneficial for all patients in clinical practice.3 The gene discussed is ACE; the disease is myocardial infarction.