However, at the stage of cancer progression, the activating mutations in Nrf2 and loss-of-function mutations in Keap1 lead to the disruption of Keap1-Nrf2 binding and constitutive activation of Nrf2, increasing the expression of genes necessary for cancer cell proliferation, ferroptosis, angiogenesis, senescence, autophagy, angiogenesis, drug resistance, and metastasis [59]. This evidence concerns the gene NFE2L2 and cancer.