A hallmark feature of many cancer cells is their increased uptake and metabolism of glucose compared to non-cancerous cells from the same origin. Cancer cells generally use a greater proportion of incoming glucose for non-oxidative purposes including the production of building blocks for cell division (lipid, DNA and protein), rather than oxidative pathways that produce carbon dioxide in mitochondria. This talk will focus on our recent efforts to target potential metabolic vulnerabilities in obesity-related cancers including blocking cancer-specific glucose uptake and the metabolic pathway that converts glucose to lipid (lipogenesis).