In cancer cells, because of chemical modifications of KEAP1 cysteine residues, the inhibition of ubiquitin conjugation to NRF2 by the KEAP1-CUL3 complex leads to NRF2-KEAP1 impairment and results in the nuclear accumulation of the de novo synthesized NRF2 protein [7,8]. The gene discussed is KEAP1; the disease is cancer.