These redox-mediated protective effects of HT are complemented by reductions in SREBP-1c expression, mitochondrial abnormalities, and apoptosis [19], besides diminution of ER stress induced by tunicamycin in human liver cells [62], with suppression of cell growth in human hepatocellular carcinoma cells via inactivation of AKT and nuclear factor-κB (NF-κB) pathways [63]. The gene discussed is NFKB1; the disease is hepatocellular carcinoma.