Based on the enrichment analyses of USP15-high AML, our previous finding linking USP15 to the hematopoietic cell stress response, and reports that the redox sensor KEAP1 is a relevant substrate regulated by USP15, we hypothesized that impinging USP15 in AML cells would modulate the KEAP1-NRF2 pathway, thus affecting cellular redox homeostasis (Fig. 4C). This evidence concerns the gene KEAP1 and acute myeloid leukemia.