AngII directly facilitates apoptosis and the skeletal reconstruction of pulmonary microvascular endothelial cells, subsequently accelerating the disruption of the pulmonary microvascular endothelial barrier and leading to more pulmonary exudate and edema [64], which likely share the characteristics of the pathological manifestations of COVID-19 patients and, therefore, are assumed to be linked to the pathogenesis of COVID-19. The gene discussed is AGT; the disease is COVID-19.