The article introduces a novel form of non-apoptotic cell death called ferroptosis, which is triggered by the oncogenic RAS-selective lethal small molecule erastin. Ferroptosis is characterized by iron-dependent, oxidative stress and is distinct from apoptosis, necrosis, and autophagy. The study identifies ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices. Ferroptosis is regulated by specific genes, including RPL8, IREB2, ATPSG3, CS, TTC35, and ACSF2. The mechanism of ferroptosis involves the inhibition of cystine uptake by the cystine/glutamate antiporter (system x_c^−), leading to a void in the cell's antioxidant defenses and the accumulation of lipid reactive oxygen species (ROS). The article also discusses the potential clinical applications of ferroptosis in cancer therapy and neuroprotection.The article introduces a novel form of non-apoptotic cell death called ferroptosis, which is triggered by the oncogenic RAS-selective lethal small molecule erastin. Ferroptosis is characterized by iron-dependent, oxidative stress and is distinct from apoptosis, necrosis, and autophagy. The study identifies ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices. Ferroptosis is regulated by specific genes, including RPL8, IREB2, ATPSG3, CS, TTC35, and ACSF2. The mechanism of ferroptosis involves the inhibition of cystine uptake by the cystine/glutamate antiporter (system x_c^−), leading to a void in the cell's antioxidant defenses and the accumulation of lipid reactive oxygen species (ROS). The article also discusses the potential clinical applications of ferroptosis in cancer therapy and neuroprotection.