NRF2 stabilization most commonly occurs via activating mutations and copy number amplifications of the NFE2L2 gene or inactivating mutations or deletions in KEAP1 or CUL3. In cancer, somatic mutations in NFE2L2 or its negative regulator KEAP1 are associated with poor outcomes in patients [9] and often confer resistance to therapy through ROS and drug detoxification [10,11]. This evidence concerns the gene NFE2L2 and cancer.