The main mechanisms of myocardial injury in patients with COVID-19 include: a cytokine storm caused by an unbalanced response of T-helper 1 (TH1 cells) and T-helper 2 (TH2 cells); respiratory dysfunction and hypoxemia; and decreased activity of ACE2, which has a protective effect on the cardiovascular system as a counterregulatory element of angiotensin II signaling [58,59]. The gene discussed is AGT; the disease is COVID-19.