WILD-seq of docetaxel-treated tumours before and after L-asparaginase treatment confirmed the specific suppression of NRF2-high clones and also revealed a compensatory, largely clone agnostic, up-regulation of asparagine synthetase (Asns), which likely drives relapse in these tumours given the importance of ASNS to L-asparaginase resistance in ALL (Richards and Kilberg, 2006). This evidence concerns the gene NFE2L2 and neoplasm.