It has been recently demonstrated that cancer cells can transcriptionally regulate NRF2 and, consequently, AKR1C1-3 activity as a pro-survival response against drug treatments.4 Thus, in order to evaluate the potential establishment of such a resistance loop in our experimental setting, we measured the amount of coumberone conversion rate in all T-ALL cell lines after 24 h of treatment with ASP, VCR, Ara-C, and Dauno at sub-lethal concentrations. This evidence concerns the gene NFE2L2 and cancer.