It is also consistent with our current understanding of the pathophysiological mechanism of COVID-19 in which SARS-CoV-2’s entry into host cells is mediated by the angiotensin-converting enzyme 2 (ACE2) receptor, which stimulates the renin-angiotensin-aldosterone system and causes vascular endothelial damage followed by vasculitis (i.e., the inflammation of blood vessels), resulting in the formation of microthrombi2,6. This evidence concerns the gene ACE2 and vasculitis.