A Nature study identified FSP1 as an essential in vivo survival factor for lung adenocarcinoma, showing that inhibiting FSP1 induces ferroptosis across genetically diverse tumors and exposes a therapeutic vulnerability. Complementary research revealed that metastatic melanoma cells in lymph nodes become dependent on ferroptosis suppression due to low free iron, elevated oleic acid and hypoxia in that microenvironment. Both papers map actionable dependencies in tumor redox biology and support development of ferroptosis-targeted therapies.