Tumor wet-weight was significantly lower in mice with CXCL12 compared to GFP control cells (Fig.10E).Consistent with the delayed cell-cycle arrest observed in vitro, immunohistochemistry revealed that CXCL12, CXCR4, and CXCR7-expressing tumors had decreased focal expression of Ki-67 compared with control tumors, indicating lower proliferative potential in vivo (Fig.10F–G). The gene discussed is ACKR3; the disease is neoplasm.