In a model of recurrent breast cancer, tumour cells that survived oxidative stress caused by oncogene inhibition did so by NRF2-directed metabolic reprogramming that entailed overexpression of genes for oxidative PPP enzymes and TXN1, TXN2 and TXNRD1, but not those for GSH synthesis, suggesting NRF2 aids formation and growth of recurrent tumours [188]. The gene discussed is TXN; the disease is neoplasm.