MRE11 and rheumatoid arthritis: In RA, reduced mitochondrial DNA biostability and mtDNA leakage into the cytoplasm due to the lack of DNA repair nuclease (MRE11A) increase the pro-inflammatory tendency of T-cells, whereas upregulation of MRE11A expression reduces mitochondrial damage and has an inhibitory effect on T-cell scorching and immune inflammation (32, 75).