Since tumor cell intravasation and extravasation depend on the disruption of tight endothelial junctions, it is reasonable to speculate that once in circulation and under certain conditions, TEVs with appropriate content (i.e., CD44, HA, miR-181c, -105, CCL2, etc.)can disrupt vascular tight endothelial junctions enabling the docking and passage of disseminating cancer cells. The gene discussed is CD44; the disease is neoplasm.