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Consequence of Nrf2 upregulation during tumorigenesis The above data suggest that although the upregulation of Nrf2 in cancer seems paradoxical, it is not an inconsequential observation or artifact—the mutations seen are specifically targeted to activate and cause accumulation of Nrf2, either by increasing stability of the transcription factor (by inhibiting its primary negative regulator Keap1 or suppressing repression by β-TrCP) or by increasing transcription of NFE2L2

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This approach not only targets the underlying genetic risk factors but also helps tailor therapies based on how an individual’s genetic makeup influences disease progression and response to treatment