In a complementary way, we treated CCRF-CEM with the redox-cycling agent t-BHQ, known to induce transcriptional activation of NRF2, subsequent ARE-driven gene expression and consequent antioxidant protection.4 A short treatment of T-ALL cells with t-BHQ was sufficient to induce the overexpression of the three AKR1C isoenzymes (Fig. 5c) and a significant increase of their enzymatic activity assessed by coumberone conversion (Fig. 5d). The gene discussed is NFE2L2; the disease is acute lymphoblastic leukemia.