In the case of AML, mutations in HDACs genes have not been detected, but interestingly, it has been described how these HDAC proteins are aberrantly recruited to specific gene promoters by abnormal oncogenic fusion proteins that occur in this disease, such as PML-RARα, PLZF-RARα, or AML1-ETO, mediating aberrant gene silencing contributing to leukemogenesis [52]. This evidence concerns the gene HDAC9 and acute myeloid leukemia.