Activation of cell membrane-associated kinases (growth factor receptors such as EGFR, which is known to affect pathogenesis and prognosis of glioma) is thought to disrupt these complexes and to promote beta-catenin transactivation and cell migration [11] independently of the Wnt pathway [12] although crosstalks may exist between them [13]. This evidence concerns the gene CTNNB1 and glioma.