Several mechanisms have been implicated in this interplay between COVID-19 and arterial health, including the COVID-19-related inflammatory cascade, the interaction between the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) spike protein and angiotensin-converting enzyme 2 (ACE2), and the subsequently increased activity of angiotensin (Ang) II/Ang II receptor type 1 (AT1) [1,5,6]. The gene discussed is ACE2; the disease is COVID-19.