Furthermore, using murine models of mouse mammary adenocarcinomas and melanomas we have shown that full-length CgA and VS-1 can enhance the endothelial barrier function and reduce the trans-endothelial migration of tumor cells, thereby reducing the trafficking of cancer cells from tumor-to-blood and from blood-to-tumor/normal tissues (i.e. the metastasis and the tumor “self-seeding” processes) [19, 20]. The gene discussed is CGA; the disease is neoplasm.