NRF2 is mutationally activated in 10–30% of different solid tumors including liver, lung, stomach, colon and other cancers and mutations typically disrupt the interaction between NRF2 and its E3 ligase KEAP1 (Kelch Like ECH Associated Protein 1) directly or by impeding KEAP1 co-factors CUL3 (Cullin 3) and CAND1 (Cullin Associated and Neddylation Dissociated 1) [2,5,6,7,8]. This evidence concerns the gene KEAP1 and cancer.