Does enhanced AKT activity depend on β-catenin for a high bone mass phenotype?

Previous research has shown that when the β-catenin gene is disrupted, bone anabolism is poor, resulting in poorly formed bones. Furthermore, when the PTEN gene is disrupted, this causes a continuous accumulation of bone. By disrupting the function of both β-catenin and PTEN, the dependence of AKT activity on β-catenin may be evaluated.