Consistently, sorafenib treatment did lead to the accumulation of reactive oxygen species (ROS) in hepatoma cells, and using N‐acetylcysteine (NAC) to clear ROS markedly suppressed the activation of the PERK/eIF2α/ATF4/CHOP signaling pathway, as well as the upregulation of TRIB3, induced by sorafenib (Figure 2F–H). The gene discussed is EIF2AK3; the disease is hepatocellular carcinoma.