As an important chromatin remodeling enzyme, LSH could act as an essential inhibitor of ferroptosis in the tumorigenesis of lung cancer through interacting with WD repeat domain 76, thereby activating the lipid metabolism‐related gene glucose transporter 1, the ferroptosis‐related gene stearoyl‐CoA desaturase 1 and fatty acid desaturases 2, and LSH can be recruited to the promoter region of SLC7A11 to enhance the transcription of SLC7A11, leading to the inhibition of ferroptosis in leukemia.24, 26. This evidence concerns the gene WDR76 and lung cancer.