In several tumor histotypes, a basal activation of this transcription factor is induced, and several somatic mutations have been demonstrated to destroy the interaction between Nrf2 and its physiological inhibitor Kelch-like ECH-associated protein 1 (Keap1), thereby promoting the persistent activation of the Nrf2-mediated antioxidant/detoxifying response and tumorigenesis [138, 139]. This evidence concerns the gene KEAP1 and neoplasm.