Numerous studies have pointed to an IFN-I-rich environment in even non-lesional skin based on transcriptomic signatures of skin from SLE and CLE patients (Billi et al., 2022; Der et al., 2017; Der et al., 2019; Psarras et al., 2020), upregulation of keratinocyte IFN-κ expression in keratinocytes of CLE, SLE, and ANA +patients (Psarras et al., 2020; Stannard et al., 2017), and upregulation of IFN-stimulated genes (ISGs) such as MX1 on tissue sections in SLE, incomplete SLE, and ANA +patients (Lambers et al., 2019; Psarras et al., 2020; Reefman et al., 2008). This evidence concerns the gene MX1 and systemic lupus erythematosus.