Furthermore, the increased transcriptional activity of β-catenin results from the activation of EGFR through ERK that directly interacts with casein kinase 2 (CK2) without altering its stability and the level of phosphorylation by GSK-3β in human glioblastoma cells U-87E, U-373, and LN229 and correlates with levels of ERK1/2 activity and grades of glioma malignancy [93] (Figure 1). This evidence concerns the gene EGFR and glioma.