Mechanistic studies indicated that XIAP overexpression in high metastatic T24T cells was due to the increased XIAP mRNA stability, which was mediated by the reduction of the decreased miR-200c binding to 3ʹUTR region of XIAP mRNA, whereas CREB inactivation was responsible for attenuated miR-200c transcription in human BC cells. This evidence concerns the gene XIAP and breast cancer.