Although HDAC mutations in AML are relatively rare compared to solid tumors, HDAC proteins are abnormally recruited to oncogenic fusion proteins, such as AML1-ETO, CBFB-MYTH11, PML-RARα, and MLL-fusions, which function as vital roles in onsetting and promoting the progress of leukemogenesis (4, 13, 31). This evidence concerns the gene RARA and acute myeloid leukemia.