Howevere, in several of pathological conditions, comprising inflammation and cancer, some of the changes, such as somatic mutations in Nrf2,Keap1,and Cul3, Keap1 modification by metabolic mediators, epigenetically silencing of Keap1, Nrf2 transcriptional activation via oncogene-mediated signaling, and unusual accumulation of the proteins that disrupting the Keap1-Nrf2 interactions, lead to prolonged activation of Nrf2 [23–29]. This evidence concerns the gene NFE2L2 and cancer.