In lung cancer, the RNA‐binding protein RBMS1 directly interacts with the translation initiation factor eIF3d, thereby bridging the 3′‐untranslated region (3′UTR) and 5′‐untranslated region (5′UTR) of SLC7A11 mRNA to enhance its expression.[15] Concurrently, transcription factors ATF4 and SOX2 promote SLC7A11 expression by regulating its promoter region.[16] Wild type p53 suppresses SLC7A11 transcription, reduces cystine uptake, and promotes lipid peroxidation and ferroptosis.[17] Apart from transcriptional regulation, SLC7A11 expression is also controlled at the post‐translational level. This evidence concerns the gene SLC7A11 and lung carcinoma.