Worth mentioning are agents such as brusatol [162], halofuginone [163], and K67 [164], which directly counters “Nrf2 addiction” [165] by promoting Nrf2 degradation by multiple mechanisms, thereby sensitizing cancer cells to chemotherapeutics, or mitomycin C, which exploits the NRF2-dependent gene products for its bioactivation and is already approved for clinical use [165,166,167]. This evidence concerns the gene NFE2L2 and cancer.