The article discusses the dual role of NRF2 in cancer, acting as both a protective and pro-oncogenic factor. NRF2 is a transcription factor that regulates antioxidant systems in response to oxidative stress, and its activity is controlled by KEAP1. Under normal conditions, NRF2 is sequestered by KEAP1, but during stress, it is released and activates genes involved in detoxification and antioxidant defense. However, excessive NRF2 activation can promote tumor growth, resistance to chemotherapy, and metastasis. The review highlights the complex mechanisms of NRF2 activation and inhibition, including interactions with KEAP1, phosphorylation, and other regulatory proteins. NRF2 regulates numerous genes involved in antioxidant defense, detoxification, and metabolic reprogramming, which are crucial for cancer cell survival. While NRF2 can protect cells from oxidative damage and promote DNA repair, its overactivation can lead to genetic instability and tumor progression. The article also discusses the potential of NRF2 modulators as therapeutic agents, noting that while NRF2 activators may have chemopreventive effects, inhibitors could enhance chemotherapy sensitivity. The role of NRF2 in tumor immunology, cancer stem cells, and metastasis is also explored, emphasizing the need for a balanced approach in targeting NRF2 for cancer therapy.The article discusses the dual role of NRF2 in cancer, acting as both a protective and pro-oncogenic factor. NRF2 is a transcription factor that regulates antioxidant systems in response to oxidative stress, and its activity is controlled by KEAP1. Under normal conditions, NRF2 is sequestered by KEAP1, but during stress, it is released and activates genes involved in detoxification and antioxidant defense. However, excessive NRF2 activation can promote tumor growth, resistance to chemotherapy, and metastasis. The review highlights the complex mechanisms of NRF2 activation and inhibition, including interactions with KEAP1, phosphorylation, and other regulatory proteins. NRF2 regulates numerous genes involved in antioxidant defense, detoxification, and metabolic reprogramming, which are crucial for cancer cell survival. While NRF2 can protect cells from oxidative damage and promote DNA repair, its overactivation can lead to genetic instability and tumor progression. The article also discusses the potential of NRF2 modulators as therapeutic agents, noting that while NRF2 activators may have chemopreventive effects, inhibitors could enhance chemotherapy sensitivity. The role of NRF2 in tumor immunology, cancer stem cells, and metastasis is also explored, emphasizing the need for a balanced approach in targeting NRF2 for cancer therapy.