In bone metastasis, acetylation of KLF5 is thus an adaptive PTM event for cancer cells to grow and survive in the TGF-β-enriched bone microenvironment; and Ac-KLF5 thus functions as an effector of TGF-β signaling in organizing downstream molecules to promote osteoclastic bone resorption and expand the living space for tumor cells, adding an essential step in the vicious cycle, i.e., TGF-β/Ac-KLF5/CXCR4/IL-11. This evidence concerns the gene CXCR4 and neoplasm.