A CRISPR–Cas9 screen published in Nature Cell Biology identified vitamin B2 (riboflavin) metabolism as a modulator of ferroptosis resistance via stabilization of FSP1 and recycling of lipid antioxidants. The team led by José Pedro Friedmann Angeli found riboflavin-derived cofactors support tumor redox defenses; riboflavin depletion sensitized cancer cells to ferroptosis and roseoflavin—an antibiotic analog—triggered ferroptotic death in cell models. Ferroptosis is an iron‑dependent form of lipid peroxidation‑driven cell death; targeting cofactor pathways could weaken tumor defenses, though a selective clinical inhibitor remains unavailable.