Recently, it was shown that ephrin-B2 expressed in GSC may also play a significant role in perivascular invasion of GSCs by two mechanisms; firstly, Eph activation leads to the expulsion of these GSC within the tumour mass, which ultimately potentiates GSC motility and results in dissemination of individual cells away from the original tumour; secondly, Eph activation leads to the repression of sensitisation of these escaped GSC to the surrounding VEC-derived ephrin-B2, and thus “hijacks” the signalling pathway by which the normal vasculature inhibits the formation of tumour [7]. This evidence concerns the gene EFNB2 and neoplasm.