Under normal physiologic circumstances, TRIM21/Ro52 negatively regulates type I IFN expression via degradation of IRF3/5; however, the IRF degradation process is downregulated in anti-TRIM21/Ro52 positive SLE patients with both increased TRIM21/Ro52 mRNA and IFN levels, whereas there is no correlation in the SLE population without these antibodies. The gene discussed is IRF3; the disease is systemic lupus erythematosus.