These lipid–redox interactions intersect canonical stress pathways (e.g., KEAP1–NRF2 and NF-κB), linking chronic inflammation to mutagenesis, survival signaling, and metabolic rewiring—mechanistic scaffolding that explains why population associations between serum lipids and cancer can be directionally heterogeneous and context dependent (Figure 1) [19]. Here, KEAP1 is linked to cancer.