The reciprocal t(15;17) translocation, found in more than 95% of APL cases, leads to the formation of the PML::RARA fusion protein, an oncogenic chimeric protein that plays a central role in leukemogenesis by interfering with multiple cellular pathways, resulting in increased proliferation of myeloid progenitors and a differentiation block at the promyelocytic stage [3,4]. The gene discussed is RARA; the disease is acute promyelocytic leukemia.