Theoretically, impaired cerebrovascular autoregulation in PRES associated with COVID-19 could be related to the following factors: hypoxemia, an abrupt increase in blood pressure, angiotensin-converting enzyme 2 (ACE2) receptor-mediated endothelial dysfunction, vascular endothelial damage caused by the inflammation storm, and use of medications related to PRES. Here, ACE2 is linked to endothelial dysfunction.