In view of the central role of ACE-2 receptor in cellular viral entry of SARS-CoV-2, in combination with the importance of the renin-angiotensin-aldosterone-system (RAAS) in maintaining endothelial homeostasis, a putative effect of inhibition of ACE and AT2 on COVID-19 severity has been proposed (15–17). This evidence concerns the gene ACE and COVID-19.