Of interest, although work on T cells in RA has shown impaired glycolytic flux in these cells due to up-regulation of glucose-6-phosphate dehydrogenase [56], this metabolic reprogramming does help T cells to proliferate and differentiate toward proinflammatory T cells through insufficiently activating the redox-sensitive kinase ataxia telangiectasia mutated (ATM) [57], suggesting that each cell type requires specific metabolic changes to become pathogenic in a particular disease. This evidence concerns the gene ATM and rheumatoid arthritis.