Other options for interfering with the CD123/IL-3 signaling pathways is using mAbs to CD123 that prevent the binding of IL-3 and are cytotoxic to CD123+ AML cells.366 CSL362 was thus developed to neutralize CD123 and displays antibody-dependent cytotoxicity against AML stem cells.372 This study also demonstrated that CSL362 had increased affinity and potency compared to CSL360, another CD123 antibody therapy that lacked clear antileukemic activity in a phase I study.373 Based on its success in AML xenograft studies,372 CLS362 entered into clinical studies and was renamed talacotuzumab. This evidence concerns the gene IL3 and acute myeloid leukemia.