This is based on several lines of evidence: (1) we identified a human goblet secretory cell subset in upper airway nasal epithelium enriched for ACE2 expression to have the highest IFN-α-induced gene signature; (2) we found that IFN-α, and to a lesser extent IFN-β or IFN-γ, induced ACE2 expression in a published dataset of air-liquid interface cultures derived from human nasal epithelial cells (Giovannini-Chami et al., 2012, Ordovas-Montanes et al., 2018); (3) we extended our search through the Interferome database (Rusinova et al., 2013) and found that, in epithelial barrier tissues, type I IFNs upregulate ACE2 in multiple studies, especially in primary bronchial cells and keratinocytes (Rusinova et al., 2013); (4) we found two STAT1 binding sites in the promoter of ACE2; (5) in our unpublished atlas of SHIV-infected macaques, known to have elevated amounts of chronic IFN signaling, we found ACE2 upregulation in absorptive enterocytes; (6) we directly provided evidence for IFN-α, and to some extent IFN-γ, inducing ACE2 expression in primary human upper airway basal cells; and (7) influenza infection in humans, a known inducer of the IFN pathway, leads to increased ACE2 expression in goblet secretory cells of the nasal epithelium (Cao et al., 2020).