As a collective consequence, the inflammatory malignant transformation into carcinogenesis and cancer progression should take place in the Nrf1-deficient cases, in which hyperactive Nrf2 acts as a potent tumor promotor, because malgrowth of the Nrf1α-/- -driven tumor in xenograft model mice was significantly suppressed by silencing of Nrf2 265. This evidence concerns the gene NRF1 and cancer.