Our results also demonstrate that in PTX-resistant breast cancer cell lines, either direct inhibition or indirect reduction of AURKB phosphorylation levels [including shRNA knockdown of AURKB expression, direct inhibition of AURKB activity using hesperadin, mutation of AURKB phosphorylation site (Fig. 3e), or use of PRKCE siRNA or PRKCE inhibitor BIM to indirectly inhibit AURKB phosphorylation] are effective in reversing cellular drug resistance. This evidence concerns the gene AURKB and breast carcinoma.