CXXC5 and acute myeloid leukemia: Previous studies in other experimental models suggest that pharmacological inhibition of anti-apoptotic intracellular signaling in human AML cells can induce apoptosis or increase proapoptotic effects of chemotherapy [22-26]; therapeutic targeting of CXXC5/RINF may therefore represent a novel and alternative strategy to increase proapoptotic activity and thereby chemosensitivity in human AML cells.