When SARS-CoV-2 binds to ACE2, internalization of the SARS-CoV-2-ACE2 complex reduced ACE2 activity, and subsequent activation of the rennin-angiotensin-aldosterone system [RAAS; higher angiotensin (Ang) II/Ang-(1–7) ratio] that may exacerbate the acute inflammatory events in COVID-19 patients and contribute to the effects of long COVID-19 (Chappell 2023). This evidence concerns the gene ACE2 and COVID-19.