In the absence of a direct role in tumour-endothelial adhesion in vivo, a CD146-mediated homotypic aggregation between metastatic melanoma cells might be important in extravasation; indeed, as tumour cell clusters (embolus formations) are more likely to become trapped within the capillary beds and lymphatic vessels, they may easily survive and establish new foci within the vascular system [59]. The gene discussed is MCAM; the disease is neoplasm.