However, our in vivo experiments using TMPRSS2-KO mice and a serine inhibitor in this study suggest that the Omicron variant, like SARS-CoV39 and other SARS-CoV-2 strains, utilizes a furin/TMPRSS2-dependent entry pathway rather than the endocytosis pathway for the infection of the airways, at least in murine models. This evidence concerns the gene TMPRSS2 and infection.