There is growing evidence that the blunted ACE2 activity resulting from the reduced expression, downregulation, and dysfunction of these receptors after viral invasion and the resulting imbalance between angiotensin II and angiotensin1–7 may play an important role in conditioning inflammatory, thromboembolic, and hemodynamic processes in patients with COVID-19 [3,4,5,33,34]. Here, ACE2 is linked to COVID-19.