Given the precedent evidence of systemic and pulmonary activation of KKS, as well as increased plasma DABK levels in COVID-19 patients [7,42,43], it is conceivable that ACE2 downregulation by SARS-CoV-2 [44,45] might upregulate the extent of B1R-dependent inflammatory edema during the course of infection. Here, BDKRB1 is linked to COVID-19.