If the TE data are available, it would be interesting to examine whether the depletion of genes related to innate immunity and autoimmunity-associated collections in the SH samples (Figure 3D) correlates with the transcriptional repression of TEs by SETDB1-involved mechanism and whether the reduced expression of nucleic acid sensors (Figure 3E) may be intertwined in this regulatory circuit. This evidence concerns the gene SETDB1 and Autoimmunity.