To elucidate how AP2M1 enhances stemness in AML, we first profiled the intensity of signaling pathways known to regulate self‐renewal, proliferation, and apoptosis of HSPCs, including Notch, Wnt, TGFβ, and Hedgehog.[29, 30, 31] Among these pathways, Notch signaling was notably the most enriched in AP2M1+ malignant HSPCs (Figure5A). This evidence concerns the gene TGFB1 and acute myeloid leukemia.