In the case of PML-RARα–driven AML, also referred to as acute promyelocytic leukemia (APL), the PML-RARα fusion protein exerts its oncogenic activity by aberrantly recruiting NuRD, PRC2, and DNMT proteins, leading to transcriptional repression of genes critical for myeloid differentiation and contributing to the characteristic differentiation block of APL (Fig. 2E) (56). The gene discussed is DNMT1; the disease is acute promyelocytic leukemia.