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Constitutive activation of NRF2, mainly via loss-of-function mutations in the CUL3-adapter KEAP1 or gain-of-function mutations in NFE2L2 , is thought to provide a fitness advantage to tumor cells in confronting metabolic/oxidative stress resulting from dysregulated growth (DeNicola et al, 2011

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= Link to IBCC section covering that topic

That shared receptor is exactly why the two are so often lumped together and why the evidence differences below are so easy to overlook