Considering that Ac-KLF5 directly activates the transcription of CXCR4 (Fig. 6), the ligand for CXCR4 (i.e., CXCL12) is enriched in the bone environment, CXCR4 promotes bone metastasis and docetaxel resistance58,80, and CXCR4 was indeed indispensable for Ac-KLF5 to promote bone metastatic lesions and docetaxel resistance (Fig. 8), combined treatments with docetaxel and CXCR4 inhibitors could prove beneficial to patients with PCa bone metastasis. Here, KLF5 is linked to posterior cortical atrophy.