The study of the effect of various XIAP inhibitors (dequalinium chloride or embelin) supported a major role for XIAP in protecting AML cells from apoptosis; particularly, these agents induced differentiation and impaired clonogenic capacity of primary AML cells [303] and synergized with TRAIL in inducing apoptosis of AML blasts [304]. The gene discussed is TNFSF10; the disease is acute myeloid leukemia.