FOXO3 and breast carcinoma: Altogether, our findings suggest that FOXK2 and its SUMOylation is crucial for the its recruitment to the FOXO3 promoter, which in turn controls the cytotoxic function of paclitaxel in breast cancer cells and that the recruitment of FOXK2 to the FOXO3 promoter is impaired in paclitaxel-resistant breast cancer cells.