Low HDAC activity in RA has previously been shown to result in hyperacetylation, which can contribute to the activation of genes coding for proinflammatory cytokines, including TNF-α and interleukin-8 (IL-8), and thus to the pathogenesis of RA [5, 15, 29, 33]. The gene discussed is CXCL8; the disease is rheumatoid arthritis.