Our previous cumulative evidences supported that activated STAT3 might be a target for anti-tumor strategy and STAT3 decoy ODN could be an ideal tool for inhibiting STAT3.[7], [8], [23] In this study, it was demonstrated that STAT3 was more activated in adriamycin resistant K562/A02 cells (Fig. 1), which was consistent with drug-resistant ovarian cancer.[15] P-gp was also frequently over-expressed in leukemia.[1] A hypothesis was that STAT3 might be involved in MDR. This evidence concerns the gene STAT3 and ovarian carcinoma.