SARS-CoV-2 is able to infect the nasal and bronchial epithelia, as well as pneumocytes, through the binding of the spike (S) protein of viral spicules to its receptor on the cell surface, which is the angiotensin-converting enzyme-2 (ACE-2); this interaction triggers an inflammatory response and, subsequently, the clinical picture of pneumonia and/or respiratory failure [1,6]. This evidence concerns the gene ACE2 and pneumonia.