The analysis of this mouse model provided evidence that the oncogenic effects of BRAF/PTEN mutants is at least in part mediated through activation of the Wnt signaling pathway: this conclusion was reached through the experimental demonstration that β-catenin loss inhibits melanoma formation in BRAF/PTEN-driven melanomas, while β-catenin stabilization accelerates BRAF/PTEN-driven melanomagenesis [14]. The gene discussed is PTEN; the disease is melanoma.