Interestingly, the spike protein of SARS-CoV has been demonstrated to downregulate ACE2 expression, thus resulting in over-production of angiotensin II by the related enzyme ACE.75,76 In a similar way, it could be hypothesized that SARS-CoV-2 may downregulate ACE2 receptors, thus leading to an over-production of angiotensin II, in turn enhancing IL-6 production in AT1/JAK/STAT-dependent manner, and ultimately driving to vascular inflammation and lung injury, clinical signatures of COVID-19 (Fig. 2). The gene discussed is SOAT1; the disease is COVID-19.