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Early research on ferroptosis-characteristic cell death is dated back to the 1950s and 1960s, led by Harry Eagle who demonstrated that cysteine depletion reduced glutathione and led to cell death, whereas cysteine synthesis protected cell death by restoring glutathione [94,95,96]

Correspondingly, KEAP1 undergoes conformational changes and disconnects from Nrf2 under oxidative stress conditions, promoting Nrf2 translocated to nucleus and combined with antioxidant response element (ARE) to regulating the transcriptional expression of detoxification genes, thereby preventing oxidative damage, mitochondrial damage and ATP depletion [44]

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This seems to lead to a shift away from the more cytotoxic T cells