The metastatic process of prostate cancer cells (PCa cells) is functionally similar to the migrational, or homing, behavior of HSCs to the bone marrow. Numerous molecules have been implicated in regulating HSC homing, participating as both chemoattractants and regulators of cell growth. Endothelial cell–derived factors such as CCL2 act as chemoattractants and growth factors for HSCs, tumor-associated macrophages, and prostate cancer cells. Osteoblasts produce the chemokine SDF-1 (CXCL12), which further guides both HSCs and prostate cancer cells into the marrow through their expression of the CXCL12 receptor CXCR4. Both HSCs and prostate cancer cells use the cell surface protein annexin II (Anxa2) on both endothelial cells (not shown) and osteoblasts as a dock/lock mechanism into the bone microenvironment. Conceptually, prostate cancer cells act as parasites of the HSC niche by coopting HSC chemokines and attachment sites to initiate a cascade of events that result in the osteoblastic metastases observed in prostate cancer patients.