Ye et al. reported that treating HT-1080 fibrosarcoma cells with the combination of RSL3 (GPX4 inhibitor) and Cs-137γ radiation evoked marked ferroptosis while the activation of caspase-dependent cell death programs and DNA damage was only marginal, indicating that blocking GPX4 activity in tumor cells using synthetic inhibitors could synergize with the RT-induced pro-lipoperoxidation effects and creates vulnerability to ferroptosis for high-Z metal free radiosensitization 81. Here, GPX4 is linked to neoplasm.