Finally, a more recent in vitro study with RA synoviocytes shows that mitochondrial dysfunction and increased glycolysis induced by hypoxia was associated in vivo with synovial expression of several glycolytic enzymes as well as glucose transporter 1 (GLUT1) to improve uptake of glucose in RA patients with low pO2 levels [80]. This evidence concerns the gene HK1 and rheumatoid arthritis.