Two independent studies exposed ferroptosis suppression as a therapeutic vulnerability. In lung adenocarcinoma, targeting FSP1 induced ferroptotic cell death across genetically diverse tumors and suppressed growth in vivo, positioning FSP1 inhibitors as broadly applicable agents. Separately, researchers mapped how the lymph‑node microenvironment—low iron, high oleic acid, and hypoxia—modulates ferroptosis sensitivity in metastatic melanoma and identified oxygen tension as a key regulator. Together, the findings define context‑specific molecular dependencies and suggest combination strategies (FSP1 inhibitors, microenvironment modulation) to trigger ferroptosis selectively in tumors. Why it matters: ferroptosis‑based therapies offer a new mechanistic class for solid cancers, with translational paths already supported by robust preclinical data.