Functional studies in metastatic MDA-MB-231 breast cancer models demonstrate that uPAR–β1 integrin complexes are present in vivo and that disruption of this interaction, via administration of a blocking peptide (p25), significantly impairs tumor progression and bone metastasis in xenograft models, confirming the essential role of uPAR in integrin-mediated adhesion and dissemination [68]. The gene discussed is PLAUR; the disease is breast cancer.