Importantly, NRF2 behaves as a “double-edged sword” in cancer biology: while its transient activation preserves genomic stability and prevents carcinogen-induced transformation during early stages of development, its persistent or constitutive activation—often driven by KEAP1, NFE2L2, or CUL3 alterations— supports oncogenesis in advanced tumors by promoting metabolic rewiring, epithelial–mesenchymal transition (EMT), invasion, and therapeutic resistance [3]. Here, KEAP1 is linked to cancer.