The vast majority(>95%) of patients with acute promyelocytic leukemia (APL) are characterized with a specific chromosomal translocation t(15,17)(q22,q21), which fuses the promyelocytic leukemia (PML) gene located on chromosome 15 to the retinoic acid receptor a(RARα) gene located on chromosome 17.[1,2] So far, typical APL with PML-RARα has responded well to all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). The gene discussed is RARA; the disease is leukemia.