As previously shown, the recruitment of N‐cadherin to heterocellular contacts plays an important role in the interaction of melanoma cells with non‐cerebral endothelial cells during transendothelial migration.17, 33 Moreover, after long‐lasting interactions, tumour cells are able to up‐regulate N‐cadherin expression in CECs during endothelial‐mesenchymal transition to enhance transendothelial migration.18 Here we show that N‐cadherin is mainly involved in melanoma‐endothelial interactions, but is dispensable in the transendothelial migration of breast cancer cells both in vitro and in vivo. Here, CDH2 is linked to neoplasm.