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The impact of changed redoxin function on ferroptosis could also be based on secondary effects, e.g., the increase in superoxide formation upon loss of mitochondrial redoxins [90,91] or activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway [92,93] , a major regulator of transcription of antioxidant and anti-ferroptotic enzymes [65]

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However, overexpression of Keap1 was shown to repress the nuclear accumulation and transcriptional activity of Nrf2, while the addition of phase II inducers, which could upregulate Nrf2, was able to relieve this repression

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