As one of AKT downstream targets, Glycogen synthase kinase 3β (GSK3β) could be phosphorylated at Ser9 and inactivated by AKT directly, potentially leading to Wnt-independent β-catenin stabilization which is well known to play a pivotal role in tumor invasion and metastasis in various cancer cells [27–29]. The gene discussed is AKT1; the disease is cancer.