Ferroptosis is a regulated form of necrotic cell death that is caused by the accumulation of oxidized phospholipids, leading to membrane damage and cell lysis 1 , 2 . While other types of necrotic death such as pyroptosis and necroptosis are mediated by active mechanisms of execution 3 – 6 , ferroptosis is thought to result from the accumulation of unrepaired cell damage 1 . Previous studies suggested that ferroptosis has the ability to spread through cell populations in a wave-like manner, resulting in a distinct spatiotemporal pattern of cell death 7 , 8 . Here we investigate the mechanism of ferroptosis execution and discover that ferroptotic cell rupture is mediated by plasma membrane pores, similarly to cell lysis in pyroptosis and necroptosis 3 , 4 . We further find that intercellular propagation of death occurs following treatment with some ferroptosis-inducing agents, including erastin 2 , 9 and C’ dot nanoparticles 8 , but not upon direct inhibition of the ferroptosis-inhibiting enzyme Glutathione Peroxidase 4 (GPX4) 10 . Propagation of a ferroptosis-inducing signal occurs upstream of cell rupture, and involves the spreading of a cell swelling effect through cell populations in a lipid peroxide- and iron-dependent manner.