However, when endothelia are situated within tumor tissues where tumor cells release factors to trigger angiogenesis with altered junctional compositions [154,155], hyperpermeability of tumor vessels renders pro-tumor leukocyte recruitment and persistent influx of plasma molecules, e.g., FN and fibrin, into chronic inflammatory TMEs, consequently facilitating tumor growth, migration/invasion, and intravasation [149,153,156,157,158]. The gene discussed is FN1; the disease is neoplasm.