A number of researchers have studied the effect of expressing mutant hyperactive forms of NRF2, modelled on somatic mutants of NFE2L2 identified in clinical lung cancer samples (e.g., Nrf2E79Q and Nrf2ΔNeh2), and none of these have provided evidence that chronic Nrf2 hyperactivity is sufficient to initiate tumourigenesis. The gene discussed is NFE2L2; the disease is lung cancer.