It may be suggested that an elevation of Ang II in a setting where ACE2 becomes diminished due to shedding from the cell surface after binding the SARS-CoV-2 virus [83,84], leads to an imbalance of the RAS system, veered towards the Ang II pathway, which may exacerbate systemic and pulmonary hypertension, with resulting cardiotoxic effects and respiratory compromise [85]. This evidence concerns the gene ACE2 and pulmonary arterial hypertension.