Meanwhile, downregulation of GSK-3β, p-GSK-3β, β-catenin and their downstream, c-Myc and cyclin D1 using the Chr-A treatment indicates that Chr-A may exert anti-glioblastoma activity by downregulating the Akt/GSK-3β/β-catenin pathway (Figure 5). The gene discussed is MYC; the disease is glioblastoma.