NFE2L2 and neoplasm: Just such loss of Nrf1α function in Nrf1α−/− cells (albeit hyper-active Nrf2 is accumulated), enabled the resultant tumorigenicity to become significantly higher than that of Nrf1/2+/+-tumor, but rather was much strikingly suppressed by silencing of Nrf2 (in the Nrf1α−/−+siNrf2-derived tumors) to the much less extent than that of Nrf1/2+/+ control cells (Figure 6A–C).