In general, when key mechanisms of inflammation are recruited, i.e., ADAM-17 releasing soluble ACE2 from cell membranes and, mostly, TNF-α downregulating cell membrane ACE2, the strategy of replacing the Ang1-7 tissue production through ACEis, NEP, and its substrate Ang I, as we illustrate in this paper, might be of some use and is worth being evaluated through trials in human patients, not only in COVID-19 but also in acute lung injury due to hRSV and avian influenza viruses. Here, ADAM17 is linked to COVID-19.