Such atypical APL cases may harbor translocations resulting in fusions between RARα and genes such as PLZF, NuMA, NPM, and STAT5B. 5, 6, 7 Therapeutically, APL can be divided in two disease subtypes: the ATRA-responsive subtype, which includes RARα fusions with PML, NPM1, NuMA, and others; and a ATRA-unresponsiveness subtype characterized by the presence of the ZBTB16::RARα and STAT5B::RARα fusions.8 This evidence concerns the gene STAT5B and acute promyelocytic leukemia.