The ACE2 receptor is reported to be an essential contributor to SARS-CoV-2 entry into the nasopharynx and lungs and the subsequent inflammation that leads to severe acute respiratory distress syndrome.13 14 Our review examined drugs across human and animal models, and we found a number of studies reporting upregulation of ACE2 levels in response to ACE-I (n=22), ARBs (n=55), insulin (n=8), thiazolidinedione (n=7) aldosterone agonists (n=3), statins (n=5), oestrogens (n=5) calcium channel blockers (n=3) GLP-1 agonists (n=2) and NSAIDs (n=2). This evidence concerns the gene INS and acute respiratory distress syndrome.