Importantly, the GSK3β activity can be inhibited by Akt-mediated phosphorylation at Ser9 leading to the translocation of β-catenin to the nucleus [24], which in turn promotes several pro-tumor processes, including EMT, proliferation, migration, and invasion, as well as the maintenance of a stem cell-like cell fraction [41]. The gene discussed is GSK3B; the disease is neoplasm.