The major mechanisms for myocardial damage in COVID-19 patients result from a cytokine storm due to unbalanced response of T-helper 1 (TH1 cells) and T-helper 2 (TH2 cells) [33]; respiratory dysfunction and hypoxemia; and decreased ACE2 activity, exerting a protective effect on the cardiovascular system as an arm for counter-regulating angiotensin II signaling [34]. The gene discussed is AGT; the disease is COVID-19.