To maintain oxidative homeostasis, cancer cells increase the transcription of antioxidant genes by acquiring either stabilizing mutations in NRF2 or inactivating mutations in its negative regulator, KEAP1. NR0B1 is a recently identified NRF2 target that supports anchorage-independent growth in KEAP1-mutant non-small cell lung cancer (NSCLC) cells. This evidence concerns the gene NR0B1 and cancer.