As the respiratory tract is the initial and primary infection site for all SARS-CoV-2 variants, we used human lung epithelial Calu-3 cells, which are both susceptible (i.e. expressing both the ACE2 receptor and the TMPRSS2 cofactor on the cell membrane) and permissive (i.e. allowing efficient viral replication with the production of high levels of viral progeny, leading to cell death) to SARS-CoV-2 infection (Tseng et al., 2005; Hoffmann et al., 2020; Rosli et al., 2021). The gene discussed is TMPRSS2; the disease is infection.