Objective Programmed cell death(PCD)plays important roles in normal biology,and its dysregulation impacts human disease.Ferroptosis,a newly emerged modality of programmed cell death driven by cell metabolism and iron-dependent accumulation of lipid peroxides,is involved in a variety of diseases including ischemic organ injuries,neurodegeneration,and cancer.The molecular basis of ferroptosis is not well defined.In this study,we show that ferroptosis can be regulated non-cell autonomously by cadherin-mediated intercellular contacts.