Restoration of KEAP1 expression in shUSP15-OCI-AML3 cells resulted in a partial rescue of leukemic progenitor function as compared to control shUSP15-OCI-AML3 cells (Fig. 5H), suggesting that functional defect of AML cells upon loss of USP15 is in part mediated by the disrupted stoichiometry of KEAP1 in the redox response. Here, KEAP1 is linked to acute myeloid leukemia.