The reported mechanisms of myocardial injury considered plausible were: hyperinflammation and cytokine storm, mediated through pathologic T cells and monocytes, leading to myocarditis; respiratory failure and hypoxemia resulting in damage to cardiac myocytes; downregulation of ACE2 expression and subsequent protective signaling pathways in cardiac myocytes; hypercoagulability and development of coronary microvascular thrombosis; diffuse endothelial injury; and inflammation and/or stress causing coronary plaque rupture or supply-demand mismatch leading to myocardial ischemia/infarction (MI). This evidence concerns the gene ACE2 and myocardial infarction.