Given that the majority of cells robustly upregulating ACE2 were epithelial, this observation potentially explains why previous analyses to define canonical ISGs within immune populations did not identify ACE2 as an induced gene. Furthermore, using both Transcription Factor database (TRANSFAC) data hosted by the interferome database, as well as chromatin immunoprecipitation sequencing (ChIP-seq) data (provided by the ENCODE Factorbook repository), we found evidence for STAT1, STAT3, IRF8, and IRF1 binding sites within −1500–500 bp of the transcription start site of ACE2 (all in human studies, Figure S4B) (Gerstein et al., 2012, Matys et al., 2003, Wang et al., 2012, Wang et al., 2013). This finding is supportive of our current hypothesis that ACE2 represents a previously unappreciated ISG in epithelial cells within barrier tissues.