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We propose that an imbalance in the action of ACE1\u2010 and ACE2\u2010derived peptides, thereby enhancing angiotensin II (Ang II) signalling is primary driver of COVID\u201019 pathobiology. ACE1\/ACE2 imbalance occurs due to the binding of SARS\u2010CoV\u20102 to ACE2, reducing ACE2\u2010mediated conversion of Ang II to Ang peptides that counteract pathophysiological effects of ACE1\u2010generated ANG II. This hypothesis suggests several approaches to treat COVID\u201019 by restoring ACE1\/ACE2 balance: (a) AT receptor antagonists; (b) ACE1 inhibitors (ACEIs); (iii) agonists of receptors activated by ACE2\u2010derived peptides (e.g. Ang (1\u20137), which activates MAS1); (d) recombinant human ACE2 or ACE2 peptides as decoys for the virus. Reducing ACE1\/ACE2 imbalance is predicted to blunt COVID\u201019\u2010associated morbidity and mortality, especially in vulnerable patients. Importantly, approved AT antagonists and ACEIs can be rapidly repurposed to test their efficacy in treating COVID\u201019.<\/jats:p><\/jats:sec><jats:sec><jats:title>LINKED ARTICLES<\/jats:title><jats:p>This article is part of a themed issue on The Pharmacology of COVID\u201019. 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