Aberrant binding of HDACs at specific promoter regions suppresses normal functional gene transcription, inducing malignancy, such as promyelocytic leukemia–retinoic acid receptor-α (PML–RARα) fusion proteins that reactivate HDACs and inhibit the expression of genes associated with hematopoietic cell differentiation, leading to the progression of acute promyelocytic leukemia (APL)70. This evidence concerns the gene PML and acute promyelocytic leukemia.