In pediatric ependymoma a positive correlation between higher co-expression of ErbB2 and ErbB4 and tumor proliferative activity has been described.[39] Furthermore, ligand-dependent activation of ErbB receptor-signaling in cultured ependymoma cells resulted in Akt phosphorylation and cellular proliferation that was significantly blocked in a dose-dependent manner using WAY-177820, an inhibitor of ErbB2 tyrosine kinase activity.[39] The present study showed especially EGFR expression compared with the other ErbB family members. This evidence concerns the gene AKT1 and neoplasm.