Of note, recent studies have shown that MRE11A, in addition to its DNA repair activity, plays a critical role in mitochondria protection, as the deficiency of MRE11A in RA T cells disrupted mitochondrial oxygen consumption; suppressed ATP generation; caused leakage of mitochondrial DNA into the cytosol; and induced inflammasome assembly, caspase-1 activation, and pyroptotic cell death [147]. The gene discussed is MRE11; the disease is rheumatoid arthritis.