However, it remains unknown whether COVID-19 has a causal relationship with intracranial hemorrhages through ACE2 inactivation, endothelial dysfunction/degeneration, coagulopathy, or hypocoagulability, or rather, whether secondary effects of COVID-19, such as renal failure, and concomitant therapeutic anticoagulation in a critically ill population is the culprit. This evidence concerns the gene ACE2 and kidney failure.