Since the SARS-CoV outbreak, the pivotal role of ACE2 as a protective factor has been described in COVID-19 (68); however, in spite of ACE2 being the receptor for these viruses, there is a decrease in the abundance of these proteins on the surface, their expression and their enzymatic action by the binding of coronavirus protein S. This is due in part to their detachment and internalization (68), with the consequent increase of Ang II, leading to more severe pathology of ARDS and greater acute lung injury (68, 78). This evidence concerns the gene ACE2 and acute respiratory distress syndrome.