As genes downstream of NRF2 signaling, the γ‐GCL subunits GCLC and GCLM are often upregulated in solid tumors which predicts poor prognosis.[41, 42] Increased GCLM and GCLC levels could enhance glutathione concentration, which blunts the impact of ROS and confers resistant to chemotherapy treatment in cancer cells.[43] However, the NRF2 pathway is often inactivated or inhibited in liver diseases such as NAFLD,[11, 12] and little is known about how HCC cells control glutathione synthesis during the NAFLD to HCC progression. This evidence concerns the gene GCLC and metabolic dysfunction-associated steatotic liver disease.