In hematologic malignancies, the oncogenic output of DDX5 appears context-dependent: in T-cell acute lymphoblastic leukemia (T-ALL) it associates with the MAML1 coactivator of Notch signaling but is dispensable for proliferation, whereas in acute promyelocytic leukemia (APL) and acute myeloid leukemia (AML), where expression levels are higher, DDX5 activity is essential for cell survival. The gene discussed is MAML1; the disease is acute promyelocytic leukemia.