Systematic CNV assessment revealed directional coordination across 24 FRDEGs wherein amplifications selectively targeted ferroptosis drivers (e.g., ALOX15, IFNG; lipid peroxidation mediators19 while deletions affected suppressors (e.g., CDKN2A, SLC40A1; antioxidant regulators20, collectively enhancing ferroptosis susceptibility in DLBCL subtypes. This evidence concerns the gene CDKN2A and diffuse large B-cell lymphoma.