Hajiasgharzadeh et al. (2019) showed that SARS-CoV also promotes TACE-dependent cleavage of ACE2 in plasma-membrane adding to ACE2 shedding and to a decrease of local ACE2 availability and activity. A demonstration, that S-protein-dependent loss of ACE2 activity could facilitate the progression of lung inflammation, was given by experiments showing that the S-Fc fusion protein causes functional imbalance of the RAS mechanisms worsening the lung damage induced by acid aspiration in mice: this worsening effect is prevented with AT1 receptor antagonists (Su et al., 2010). Here, ACE2 is linked to inflammation.