NRF2 represents a Janus face in tumor biology [116]: while, on the one hand, helping to prevent malignant transformation in the first place (Nrf2 deficiency results in tumor initiation in mice [117], and loss of NRF2 activity due to BRCA1 deficiency has been suggested to contribute to (early-onset) carcinogenesis [95]), excessive NRF2 activation helps tumor cells, on the other hand, to escape apoptosis by upregulating ROS-scavenging antioxidant signaling such as glutathione replenishment. Here, NFE2L2 is linked to neoplasm.