Therefore, we suggest the possibility that the high accumulation of Sema3C in glioblastomas may be the result of: i) lower activity of certain Sema3C-targetting protease(s) compared to lower grade astrocytomas or ii) the higher degree of protection of Sema3C against ECM proteases while being in a complex with cell surface receptors (neuropilins, plexins [3, 15]) in glioblastomas. This evidence concerns the gene CD177 and glioblastoma.