For example, in 2007 Weinberg and colleagues showed how the tumor environment facilitates metastatic spread by eliciting reversible changes in the phenotype of cancer cells via CCL5-CCR5 chemokine signaling involving mesenchymal stem cells.47 CCR5 also contributes to breast cancer metastasis to bone by mediating the interaction between cancer cells and fibroblasts in the bone cavity.48 As with most chemokines, CCR5 undergoes palmitoylation at three cysteine residues within its C-terminal region. The gene discussed is CCR5; the disease is breast cancer.