There are multiple mechanisms proposed [6]: (1) direct cardiac damage mediated by stimulation of the angiotensin converting enzyme 2 (ACE2), which is expressed on myocytes and vascular endothelial cells and involved as receptor for SARS-CoV-2; (2) myocardial damage induced by hypoxia; (3) damage related to systemic inflammatory response mediated by release of cytokines, the so-called “cytokine storm”; and (4) macro and microcirculatory thrombosis, correlated to a state of hypercoagulability [7]. The gene discussed is ACE2; the disease is thrombophilia.