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Under basal homeostatic conditions, Nrf2 is sequestered in the cytoplasm through its interaction with the adaptor protein KEAP1 (Kelch-like ECH-associated protein 1), which targets Nrf2 for ubiquitination and subsequent proteasomal degradation

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This protein operates by exporting Gln in exchange for other amino acids, meeting the heightened demand for protein synthesis in cells and forming the basis for the proliferation of KRAS-mutant cells

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Excessive ROS levels can induce transcription factors like nuclear factor-kappa B (NF-kB), which is accountable for regulating cell growth and oncogenesis [37, 39]