Along these lines, inhibition of upstream signaling that triggers STAT3 activation or gene knockdown of STAT3 sensitized human breast cancer cells to chemotherapy by compromising the anti-apoptotic activity of Bcl-2, thus providing support to our hypothesis that STAT3-Bcl-2 axis serves as a pro-survival mechanism and contributes to the acquisition of drug resistance phenotype [43]. This evidence concerns the gene STAT3 and breast carcinoma.