Considering the established function of NRF2 as a principal transcriptional regulator of antioxidant genes in response to oxidative stress [20, 21], along with its frequent hyperactivation in KEAP1-mutant lung adenocarcinoma [22, 23], we were prompted to investigate the role of NRF2 in mediating cisplatin resistance through the regulation of ferroptosis. The gene discussed is KEAP1; the disease is lung adenocarcinoma.