Furthermore, decreased expression of Akt-affected GSK-3β and their downstream proteins including β-catenin, c-Myc and cyclin D1 in U251 and U87-MG cells after Chr-A treatment for 48 h implied that Chr-A may exert an anti-glioblastoma action via the Akt/GSK-3β/β-catenin signaling pathway in vitro. The gene discussed is MYC; the disease is glioblastoma.