Disturbed redox metabolism is a hallmark of solid tumors, and more recently, it has been noted in hematological malignancies. In acute lymphoblastic leukemia derived from B cell precursors, we observed heightened oxidative stress alongside increased expression of specific enzymes associated with the thioredoxin system (Fidyt et al., Molecular Oncology, PMID: 30861284). Both genetic and pharmacological inhibition of these enzymes potentiated the efficacy of targeted therapies, including BCL-2 inhibitors (Fidyt et al., Oncogene, PMID: 35091682), tyrosine kinase inhibitors, and DNA repair pathway inhibitors (Komorowski et al., manuscript accepted for publication in HemaSphere journal).