Intriguingly, recent findings suggest that the ROS-scavenging activity of the p62-NRF2 axis can be circumvented by exploiting the ability of NQO1 to activate bioreductive prodrugs, in particular one named 29h, which then induces apoptosis, showing that novel targets related to the redox status of cancer cells might open promising avenues for cancer treatment [136]. Here, NFE2L2 is linked to cancer.