NRF2-KEAP1 interaction is inhibited by (1) somatic mutations in KEAP1, Cullin3 (CUL3), or NRF2 genes, including 10%–15% lung [47,48], and 8% hepatocellular [49] cancers, (2) epigenetic silencing of KEAP1 [50], (3) accumulation of KEAP1 or NRF2 interacting proteins, such as BRCA1, p62 or PALB2 [51,52,53], (4) cysteine modification of KEAP1 mediated by oncometabolites, such as fumarate [54] and itaconate [55], or (5) modification of KEAP1 by glycolysis-derived methylglyoxal [56]. Here, KEAP1 is linked to cancer.