Studying a genetically engineered mouse model, Badgley et al. [34] reported that deletion of solute carrier family 7, member 11 (SLC7A11, a system xc− subunit) induced tumour cell ferroptosis and doubled median survival compared to a vehicle treatment, and mice treated with the antioxidant N-acetyl cysteine (NAC) exhibited restoration of baseline survival and elimination of tumour responses, supporting a link to cyst(e)ine metabolism. The gene discussed is SLC7A11; the disease is neoplasm.