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We have also described the ambiguous role played by Nrf2 in cancer insofar that although in rodents it mediates the benefits of cancer-chemopreventive agents against many chemical carcinogens, it also seems to support Kras G12D -driven carcinogenesis in mouse tumor models and it is constitutively upregulated in many human tumors through somatic loss-of-function mutations in Keap1 and PTEN and gain-of-function mutations in NFE2L2 and KRAS

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This means you can extend cycles if needed or stop at any point without withdrawal effects or rebound issues