Moreover, both in vitro and in vivo experiments—including subcutaneous and orthotopic lung tumor models—demonstrated that Cu-DMSA-HA NPs promoted intracellular ROS accumulation, mitochondrial disruption, GSH depletion, and downregulation of glutathione peroxidase 4 (GPX4) expression levels, ultimately triggering ferroptosis in cancer cells. This evidence concerns the gene GPX4 and cancer.