Using immunofluorescence staining the authors indicated that elevated expression of ADAM17 at the invasive front was associated with the presence of CD133+ GSCs in human glioblastoma via activation of the EGFR/PI3K/AKT signaling pathway (EGFR ligand-binding induces receptor self-dimerization, autophosphorylation and subsequently activates downstream PI3K/AKT) [76]. Here, AKT1 is linked to glioblastoma.