If this is indeed the case and also applicable for paclitaxel resistance acquired by ovarian cancer after paclitaxel chemotherapy, the therapeutic strategy targeting CEPB4/CSAG2 axis, such as genetically reducing their expression or chemically inhibiting their activities, may thus be of potential clinical benefits for reducing paclitaxel resistance and enhancing the cytotoxic response of ovarian cancer to paclitaxel treatment. This evidence concerns the gene CSAG2 and ovarian carcinoma.