This suppression of autoimmunity is consistent with a recent hypothesis stating that SETDB1 overexpression tightly seals off the expression of various genomic TEs, thus blocking self-retroelement-derived nucleic acids (RdNAs) to be piled up in the cytoplasm, which can cause autoimmune diseases such as Aicardi-Goutieres syndrome (Volkman and Stetson, 2014). Here, SETDB1 is linked to Aicardi-Goutières syndrome.