MRE11 and rheumatoid arthritis: CD4+ T cells serve as a proinflammatory effector in RA; Li et al. evaluated the function of DNA repair nuclease MRE11A in RA and found that MRE11A deficiency led to metabolic abnormalities accompanied by ROS, reduced ATP and the leakage of mitochondrial RNA (mtRNA), which further promoted T cell pyroptosis and tissue inflammation [93].