KLF5 and neoplasm: Considering that Ac-KLF5 and CXCR4 plays a role in docetaxel resistance in some cancers56–59; and we have observed that CXCR4 is transcriptionally upregulated by KLF5KQ (Fig. 6), the Ac-KLF5/CXCR4 axis plays a necessary role in tumor-induced osteoclast differentiation (Fig. 5), and Ac-KLF5 promoted bone metastatic growth (Fig. 2), it is plausible that CXCR4 expression induced by KLF5KQ mediates the resistance of KLF5KQ-expressing bone metastases to docetaxel.