Acute promyelocytic leukemia (APL) constitutes approximately 10–15% of the total cases of AML [70] characterized by genetic rearrangements involving the retinoic acid receptor, alpha (RARA) gene, and either promyelocytic leukemia (PML) or promyelocytic leukemia zinc finger (PLZF) gene, in APL cases with PML/RARA fusions, treatments with arsenic trioxide and all-trans retinoic acid (ATRA) target the fusion protein for degradation through the proteasome, leading to cellular differentiation and clinical remission. This evidence concerns the gene ZBTB16 and acute myeloid leukemia.