The mechanism by which CWSs could develop during COVID-19 recovery remains unclear; however, several hypotheses have been postulated to explain their development during the acute infection, including occlusive vasculopathy, angiotensin-converting enzyme 2 (ACE2) downregulation by SARS-COV-2, hypercoagulopathy, or an immune complex deposition in the vessel walls [11]. Here, ACE2 is linked to COVID-19.