Acute promyelocytic leukemia (APL), a subtype of acute myeloid leukemia, is characterized at the molecular level by the presence of the fusion gene of PML (promyelocytic leukemia) and RARA (retinoic acid receptor alpha), which arises from the t(15;17)(q24;q21) chromosomal translocation.1,2 This cytogenetic abnormality leads to the production of an oncogenic fusion protein that disrupts the critical pathways regulating myeloid cell differentiation, particularly by inhibiting the normal transcriptional activity of RARA-targeted genes. The gene discussed is RARA; the disease is acute myeloid leukemia.