Mechanistically, uPAR forms functional complexes with vitronectin-binding integrin αvβ3 on osteoclasts and tumor cells, coordinating with Src-family kinases to activate downstream signaling (e.g., c-Src, Pyk2, p130Cas) that enhances osteoclast differentiation, extracellular matrix degradation, and tumor cell colonization in bone metastasis models [118]. The gene discussed is PLAUR; the disease is neoplasm.