Postulated mechanisms for the presumed low risk for severe COVID-19 included protective effects of known low ACE2 levels in PAH, resulting in decreased viral entrance in the lung cells, mitigation from the COVID-19 cytokine storm afforded by the chronic inflammatory milieu of PAH, or theoretical (and controversial) hemodynamic beneficial effects on the ventilation/perfusion matching in COVID pneumonia/ARDS of specific PAH medication [5,6,7,8,9]. Here, ACE2 is linked to acute respiratory distress syndrome.