Major mechanisms involved in the development of thrombosis in COVID-19 include endothelial damage due to inflammation, cytokine-mediated immunopathological responses, lymphocyte cell death, hypoxia [46], oxidative stress, direct viral infection of endothelial cells [13,47], hypercoagulation [48], dysregulation of the renin-angiotensin-aldosterone system and the role of ACE2, and activation of von Willebrand factor [49]. Here, ACE2 is linked to COVID-19.