To further investigate the influence of soluble CXCL9 during endothelial breakdown and to detect whether the melanoma cells were able to form holes, which could be due either by increased endothelial apoptosis/necrosis and/or by cell–cell contact disruption during transmigration in the endothelial monolayers, HUVECs were grown to confluence and were subsequently stimulated with 200 ng ml−1 soluble CXCL9. Here, CXCL9 is linked to melanoma.