Cornelia [38] found that T cells from RA patients have an impaired TCA cycle due to the absence of the mitochondrial protein SUCLG2, which leads to the accumulation of excess acetyl coenzyme A and causes acetylation of the microtubule system, ultimately promoting the migratory behavior of T cells and disrupting the body's immune tolerance. The gene discussed is SUCLG2; the disease is rheumatoid arthritis.