Although the molecular mechanisms mediating these effects are not entirely clear, the activity of the PI3K/AKT, MAPK, and FAK pathways (all of which promote cell proliferation and/or adhesion) increase upon TNC silencing, implicating that this ECM protein may be involved in the maintenance of the GBM invasive niche and promotion of tumor cell invasion [104, 127]. This evidence concerns the gene AKT1 and glioblastoma.