Articleshttps://doi.org/10.1038/s41556-018-0178-01DepartmentofExperimentalRadiationOncology,TheUniversityofTexasMDAndersonCancerCenter,Houston,TX,USA.2DivisionofBiostatistics,DanL.DuncanCancerCenterandDepartmentofMolecularandCellularBiology,BaylorCollegeofMedicine,Houston,TX,USA.3DepartmentofTranslationalMolecularPathology,TheUniversityofTexasMDAndersonCancerCenter,Houston,TX,USA.4DepartmentofCancerBiology,ClevelandClinicLernerResearchInstitute,Cleveland,OH,USA.5TheUniversityofTexasMDAndersonUTHealthGraduateSchoolofBiomedicalSciences,Houston,TX,USA.6DepartmentofMolecularandCellularOncology,TheUniversityofTexasMDAndersonCancerCenter,Houston,TX,USA.7GraduateInstituteofBiomedicalSciencesandCenterforMolecularMedicine,ChinaMedicalUniversity,Taichung,Taiwan.8Presentaddress:InstituteofBiology,WestlakeUniversity,Hangzhou,ZhejiangProvince,China.9Presentaddress:GuangdongKeyLaboratoryofLiverDiseaseResearch,TheThirdAffiliatedHospitalofSunYat-SenUniversity,Guangzhou,China.10Theseauthorscontributedequally:YileiZhang,JiejunShi.*e-mail:WL1@bcm.edu;bgan@mdanderson.orgTosurvive,cancercellsrequireanadequatesupplyofnutrients,suchasaminoacids,tomaintainredoxhomeostasisandtomeettheirbiosyntheticandbioenergeticneeds1,2.Nutrientdepletioninducesmetabolicstressandeventuallyprovokescelldeath,includingapoptosisandothernon-apoptoticformsofregu-latedcelldeath3,4.Cancercellsengagestrategiesofmetabolicadapta-tion,includinginactivationofapoptosispathways,tosurviveundermetabolicstressconditionsandtoallowtumourprogression5,6.Itisconceivablethatnon-apoptoticcelldeathpathwaysarealsodys-regulatedincancer,althoughtheunderlyingmechanismsremainmuchlessunderstood.Ferroptosisisarecentlyidentifiedmetabolicstress-inducednon-apoptoticformofregulatedcelldeaththatiscausedbycys-tinedepletionandoverproductionoflipid-basedreactiveoxygenspecies(ROS),particularlylipidhydroperoxide,inaniron-depen-dentmanner7–11.Solutecarrierfamily7member11(SLC7A11,alsocalledxCT),thecatalyticsubunitofthecystine/glutamateantiportersy...
