The tumor suppressor PTEN promotes APC/C-Cdh1 activity (127, 134) and cells from mice that overexpress PTEN show APC/C-Cdh1-mediated degradation of PFKFB3 and glutaminase, resulting in a decrease of glycolysis and proliferation, and an increase in resistance to oncogenic transformation (127). The gene discussed is PTEN; the disease is neoplasm.