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Activation of the UPR generally serves as a readout for ER stress, but it is not clear what diminished ER stress implies in terms of an actual accumulation of unfolded proteins, particularly because some stressors, such as palmitate loading, activate the UPR apparently independent of the protein folding process (Volmer et al., 2013)

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These links support the view that -oxidation, when present, helps restrain ferroptosis by limiting the available PUFA pool, and that targeting PUFA oxidation or these parallel antioxidant systems can sensitize solid tumors to ferroptotic cell death