Given the observation that system-wide imbalances in the ACE:ACE2 ratio favouring the pro-inflammatory ACE axis are commonly observed in certain disease states commonly comorbid in severe COVID-19, it could be hypothesised that immune dysregulation of the RAAS and associated increases in pro-inflammatory mediators in the lungs may play a central role in the pathophysiology of SARS-CoV-2, such as induction of acute lung injury (ALI) or ARDS—both of which are notable causes of death in critically ill patients suffering from COVID-19 (Wu et al. 2020). Here, ACE2 is linked to COVID-19.