The key points emphasize that: (1) evolutionary affinity of SARS-CoV2 to ACE2 determines the virus-cell permissiveness and host species tropisms [20,65]; (2) the binding of the viral spike protein (S) to ACE2 inhibits and disrupt angiotensin (Ang) conversion and relevant Ang humoral homeostasis; and (3) the RAAS is then diverted to physio-pathological induction of vasoconstriction, hypertension, fibrosis, oxidative stress, and proinflammation [62,63,64,65,66,67,68,69,70,71]. The gene discussed is ACE2; the disease is hypertensive disorder.