COVID-19 is characterized by fever, cough, shortness of breath, myalgia, and headache. The disease also takes a more severe form with life-threatening manifestations of acute respiratory distress syndrome (ARDS), acute cardiac injury, acute kidney injury, disseminated intravascular coagulopathy, and cytokine storm. It has been elucidated that like its predecessor, the SARS CoV, the SARS CoV-2 utilizes the ACE2 receptor to enter cells. This knowledge brought into speculation the effects of a dysregulated Renin-Angiotensin system (RAS) in the pathogenesis of COVID-19. It has been proposed that the effects of a dysregulated RAS would lead to an inflammatory cascade and contribute to the cytokine storm that is central to the disease. This paper looks at the RAS pathway and the hypothesizes the possibility of a positive RAS feedback loop in the pathogenesis of COVID-19. We also propose possible drug targets for the treatment of COVID-19.