Inhibiting these pathways (e.g., Complex I blockade) can disrupt redox homeostasis, selectively compromising NRF2/KEAP1‐mutant cancers pushed beyond their reductive tolerance limit.[24] Thus, while NRF2/KEAP1‐mutant cancers thrive on a tilted redox balance, they become selectively vulnerable if pushed past their reductive level tolerance. This evidence concerns the gene KEAP1 and cancer.