Ferroptosis is a novel, non-apoptotic type of cell death displaying unique features and is involved in various diseases including cancer. Ferroptosis is an oxidative, iron-dependent form of cell death and is distinct from apoptosis, classic necrosis, autophagy and other forms of cell death. It is triggered through inactivation of glutathione (GSH)-dependent antioxidant defenses, which results in the accumulation of toxic lipid reactive oxidative species (ROS). Depletion of plasma membrane polyunsaturated fatty acids also occurs. Ferroptosis has been implicated in the pathological death of brain tissues exposed to high levels of glutamate, and kidney and heart tissues subjected to ischemia–reperfusion injury. With respect to cancer, ferroptosis may act as an endogenous tumor suppressive mechanism downstream of p53. Recent studies have identified a number of genes required for ferroptosis, including those involved in lipid, iron and amino acid metabolism. The ferroptosis PCR primer library contains 88 genes directed at this important cell death pathway along with 8 housekeeping genes.