The elevated autoAbs include not only previously well-documented SLE-specific anti-nuclear antibodies, e.g., anti-DNA, anti-Ro/SSA, anti-La/SSB, and anti-Smith ribonucleoproteins (Sm/RNP), but also a large number of novel autoAbs against a broad range of functional proteins, such as DNA repair enzymes, ubiquitin-related enzymes, diverse kinases, transcription regulators, translation initiation factors, interferon-related proteins, and other signaling factors. This evidence concerns the gene TRIM21 and systemic lupus erythematosus.