Further investigation of xenograft model mice showed that malignant growth of Nrf1α−/−-derived tumors is almost abolished by silencing of Nrf2, while Nrf1α+/+-tumor is markedly repressed by an inactive mutant (i.e., Nrf2−/−ΔTA), but largely unaffected by a priori constitutive activator (i.e., caNrf2ΔN). Here, NFE2L2 is linked to neoplasm.