This latter hypothesis is consistent with a recently proposed model which argues that during infection with SARS-CoV-2, ACE2 would be less available to degrade the des-Arg9-bradykinin and Lys-des-Arg9-bradykinin peptides, thereby leading to overactivation of B1R and subsequently lung angioedema (van de Veerdonk et al., 2020). This evidence concerns the gene ACE2 and infection.