In this context, it is important to emphasize that although we find that oncogenic β-catenin/WNT signaling is critically required for PIN formation in PtenS380D/D mice, it is well possible that the observed partial loss of tumor suppressive PTEN functions (as reflected in the increase in PI3K-AKT signaling and mitotic errors) cooperates with aberrant β-catenin/WNT signaling. The gene discussed is AKT1; the disease is neoplasm.