Apart from hypoxia, SARS-CoV-2’s direct penetration into myocardial cells through the receptors of the angiotensin-converting enzyme-2 (ACE-2), as well as activation of virus-triggered CD8+ T lymphocytes, might result in myocardial injury, remodeling, and adverse cardiac outcomes, seen as subclinical or overt myocarditis [30]. This evidence concerns the gene ACE2 and myocarditis.