These findings may be supported by the documented deficiency of ACE2 in the African population, which explains the high prevalence of severe symptoms and high mortality among this community with COVID-19.[31,33,35] In addition, ACE2 is involved in the inactivation of bradykinin as a component of the kallikrein-kinin system, causing pulmonary edema due to a local increase in vessel wall permeability, which increases the risk of developing ARDS, sepsis and multi-organ failure.[36]. Here, ACE2 is linked to Sepsis.