Furthermore, in these patients, upregulated expression within AtMs of the B cell receptor (BCR) signaling molecule CD79B and the IFN-inducible gene MX1 (Figure 2E, middle and right; Table S2.5) implied enhanced BCR and IFN signaling (Michalska et al., 2018), reminiscent of the hyperactive state of B cells seen in SLE (Domeier et al., 2018), and associated with the over-production of lupus autoAbs (Jenks et al., 2018). This evidence concerns the gene BCR and systemic lupus erythematosus.