Moreover, the expression of Nrf2 regulated antioxidant enzymes in AML such as glutaredoxin and thioredoxin reductase (TrxRD1) [22,23] has been shown to ‘buffer’ the AML against lethal levels of ROS, keeping the cell in a tumourigenic state that promotes cell proliferation, survival and may confer chemotherapy resistance [24,25]. The gene discussed is GLRX; the disease is acute myeloid leukemia.