During the infection, as long as the virus persists, there is dysfunction of ACE2 function, leading to the dysregulation of the kinin-kallikrein pathway and thus causing the angioedema [27]. Some evidence that the edema is bradykinin-generated includes resistance to corticosteroids, epinephrine, and antihistamines in the management of reducing the pulmonary edema in COVID-19 patients. In fact, the so called Bradykinin Storm is likely responsible for most of the observed COVID-19 symptoms.