SARs-CoV-2, the etiological agent responsible for severe acute respiratory syndrome (SARS), after binding to the angiotensin-converting enzyme-2 receptor (ACE-2), leads to endothelial dysfunction in the alveolar system and pulmonary endothelial cells, hindering the hematosis process, but also intensifies the systemic oxidative stress, insulin resistance and inflammation [14]. The gene discussed is ACE2; the disease is severe acute respiratory syndrome.