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). This evidence concerns the gene PML and acute promyelocytic leukemia.