As described for tumor-derived CXCR2, we determined the severity of osteolysis by calculating the bone destruction index and observed significant inhibition (p < 0.05) of osteolysis in Cxcr2−/− mice implanted with Cl66-Luc cells in comparison with the wild type mice (Figure 5A,B) suggesting that the scarcity of CXCR2 dependent signaling in the host may have abrogated the activation of osteoclasts. Here, CXCR2 is linked to neoplasm.