By overexpressing the methyltransferase METTL3 and treating cells with the FTO inhibitor FB23-2, we were able to regulate intracellular m6A levels and confirm that NLN modulates the expression of GPX4 by inhibiting cellular m6A modification, which leads to the degradation of GPX4 mRNA and subsequently induces ferroptosis in lung cancer cells. The gene discussed is GPX4; the disease is lung carcinoma.