GPX4 and colorectal carcinoma: Specifically, NCX4040 treatment led to increased reactive oxygen species (ROS), lipid peroxidation, and activation of ferroptosis-related genes such as CHAC1, GPX4, and NOX4. These effects were reversed by ferrostatin-1, a specific inhibitor of ferroptosis, confirming the ferroptosis-dependent nature of NO-induced cell death in CRC models (35).