This has led many clinical research teams to hypothesize that soon after infection of people, SARS-CoV-2 is likely to trigger a dysfunction of ACE2 and subsequently variations in the balance between Ang II and Ang-(1-7), contributing to worsening hypertension and releasing of proinflammatory cytokines, especially IL-6, thereby accelerating - atherogenesis (35, 51). The gene discussed is ANG; the disease is infection.