Akt is a downstream target of PI3K, and can inactivate GSK-3β by phosphorylation on serine 9.(17) Igf1−/− mice exhibit hypophosphorylated GSK-3β in the tibial growth plates.(11) Raucci and colleagues reported that IGF-1 signals induce Akt phosphorylation and promote osteoblast differentiation, and cells expressing active Akt have increased levels of stabilized β-catenin.(18) IGF-1 also regulates the location, stability, and transcriptional activity of β-catenin in cancer cells.(19). The gene discussed is GSK3B; the disease is cancer.