Another study using human embryonic kidney (HEK293T) and mouse hepatocellular carcinoma (Hepalclc7) cells pointed out that dexamethasone treatment enhanced glucocorticoid receptor (GR) recruitment to antioxidant response elements (AREs) region and subsequently blocked NRF2-dependent CREB-binding protein (CBP) recruitment and histone acetylation at AREs, which inhibited the transcriptional activation of NRF2 target genes and reduced its antioxidative function (23). The gene discussed is NR3C1; the disease is hepatocellular carcinoma.