The endocytosis of the ACE2–virus complex leads to a depletion of the plasmalemmal pool of ACE2 with a secondary reduction in conversion of angiotensin II to angiotensin 1–7; the latter peptide possesses marked anti-inflammatory properties, and its reduction significantly contributes to lung failure and to the massive occurrence of pulmonary fibrosis observed among patients with COVID-19. This evidence concerns the gene AGT and COVID-19.