In a vascular inflammation model in which HUVECs were treated with TNF-α, a factor closely associated with NF-κB, secreted acetylated-APE1/Ref-1 rapidly deacetylated and inhibited TNF-α-stimulated endothelial inflammation, suggesting that a conformational change in the extracellular domain of TNF receptor 1 is necessary to regulate TNF-α-stimulated inflammation in response to APE1/Ref-1 [140]. The gene discussed is APEX1; the disease is inflammatory response.