In melanoma cells, adhesion to vitronectin is enhanced in the presence of uPA, and soluble uPAR inhibits this effect, indicating that uPA/uPAR functions as a vitronectin receptor that can promote cell attachment (Sidenius and Blasi, 2000; Sidenius et al, 2000) In contrast, plasminogen activator inhibitor I stimulates melanoma cell migration on vitronectin, presumably either by inhibiting uPA/uPAR-mediated cell adhesion or by direct effects on the cytoskeleton (Waltz et al, 1997). This evidence concerns the gene VTN and melanoma.