Evidence for the role of TMPRSS2 in viral entry was provided by Letko et al. (2020), who demonstrated that the addition of TMPRSS2 during the course of SARS-CoV infection facilitated entry into cells that exhibit low expression of ACE2 receptors [51], and by Chupp et al. (2022), who found that treatment of patients with COVID-19 with camostat methylate, the inhibitor for TMPRSS2, reduced olfactory dysfunction [52]. This evidence concerns the gene TMPRSS2 and severe acute respiratory syndrome.