Finally, because our in vivo and in vitro work indicate that IFN might promote human cellular targets for SARS-CoV-2 infection in the human upper airway by inducing ACE2, we attempted to extend our transcriptomic data on IFN-driven expression of ACE2 to protein-level induction of ACE2. As testing of various commercially available polyclonal antibody preparations found broad evidence for non-specific or inconclusive staining in histological immunofluorescent based readouts (data not shown), we assessed whether IFN-γ-stimulated human bronchial air-liquid interface cultures induced ACE2 within 24 h. Our results show that cells from one patient robustly induced ACE2 (+2.02x), cells from another mildly induced ACE2 (+1.21x) and two patient’s cells showed minor changes (+/−1.12x) (Figure S5M). We provide a note of caution as these cells were derived from asthmatic patients, and the overall changes did not reach significance. Furthermore, we could not determine cell surface localization of ACE2 but do note that these results align with our transcriptomic data.