This could explain the lack of total inhibition of trans-endothelial migration in our study and suggest that a better understanding of the interaction between COX-2, HBEGF and ST6GALNAC5, as well as a better characterization of the complex cellular and molecular mechanisms that govern cancer cells adhesion and transmigration through the BBB are needed to optimize the therapeutic strategies that aim at suppressing breast cancer brain metastasis by inhibiting the migration of cancer cells through the brain endothelium. The gene discussed is ST6GALNAC5; the disease is breast cancer.