However, at the stage of cancer progression, the loss-of-function mutations in Keap1 and the activating mutations in Nrf2 often happen and lead to the disruption of Keap1-Nrf2 binding and the stabilization and constitutive activation of Nrf2, herein increasing the expression of genes (as summarized in Table 2) that are important for cancer cell proliferation, stem cell self-renewal, cell cycle arrest, apoptosis, ferroptosis, senescence, autophagy, angiogenesis, metastasis, drug resistance, metabolic reprogramming, genome stability and proteotoxic stress [9, 12, 18, 53–73, 75–79, 82]. The gene discussed is KEAP1; the disease is cancer.