The rapid replication of SARS-CoV-2 in the lungs, whose cells express high levels of ACE2, can trigger an intense immune-inflammatory response, leading to the development of acute respiratory distress syndrome (ARDS) in some cases, characterized by respiratory distress associated with hypoxemia and the presence of bilateral infiltrates on chest imaging, currently considered the leading cause of death in patients with COVID-19 [2,3]. Here, ACE2 is linked to acute respiratory distress syndrome.