The clinical responses seen with all-trans retinoic acid (ATRA) in acute promyelocytic leukemia (APL), subsequently found to reflect the presence of the PML-RARα translocation fusion product, and the incredible success of imatinib in t(9;22) chronic myeloid leukemia (CML), driven by the BCR-ABL tyrosine kinase, led many to believe that identifying single genetic abnormalities in myeloid cancers would predict response to targeted therapies. Here, RARA is linked to acute promyelocytic leukemia.