Apart from histone acetylation towards NFE2L2, Alam et al. (2017) have elaborated that glucocorticoids (GC) could directly inhibit histone acetylation at ARE and decrease NRF2 transcriptional activation through glucocorticoid receptor (GR) signaling, resulting in impaired NRF2-mediated antioxidant response due to the side effects of GC in hepatocellular carcinoma. The gene discussed is NR3C1; the disease is hepatocellular carcinoma.