Li Y, Zeng X, Lu D, et al. - Given an iron overloading microenvironment of ectopic endometrial stromal cells (EESCs) and their tendency to be more sensitive to oxidative damage and the characteristic of erastin-induced ferroptosis is iron-dependent accumulation of lethal lipid reactive oxygen species (ROS), researchers here examined if erastin could activate ferroptosis to regress endometriotic lesions. They recruited 11 patients without endometriosis and 21 patients with endometriosis in this study. They isolated and cultured primary normal and ectopic endometrial stromal cells and subjected them to various treatments. Ten C57BL/6 female mice were involved in the in vivo study to establish the model of endometriosis. Relative to normal endometrial stromal cells (NESCs), EESCs were identified as more susceptible to erastin treatment. Treatment of cultured EESCs with erastin led to a dramatic increase in the total ROS level (vs control), lipid ROS level (vs NESCs) and intracellular iron level (vs NESCs). Overall findings suggest that erastin could induce ferroptosis to regress endometriotic lesions in endometriosis.