Ferroptosis is proposed to result from overwhelming iron-dependent oxidative injury, which is distinct from apoptosis, necrosis, and autophagy. This iron-dependent process is marked by increased levels of cytosolic and lipid reactive oxygen species (ROS) and abnormally small mitochondria with increased membrane density. Ferroptosis is similar to glutamate-induced excitotoxicity. Recently, many reports have revealed that ferroptosis is precisely regulated by some cellular signaling pathways, like apoptosis, including regulators of iron homeostasis, RAS pathway induction of oxidase gene expression, and cystine transport impacting glutathione synthesis. Ferroptosis contributes to the process of neurodegeneration and strategy to kill RAS-mutant cancer cells.