Experimentally, the hypothesis that diabetes is a causal factor of PDAC and exerts its promoting effect through carbonyl stress, is supported by data demonstrating that hyperglycemia and AGEs dramatically accelerate and increase PDAC development in a mouse model of Kras-driven PaC [171,203] and that treatment of diabetic mice with RCS sequestering agents—and, thus, AGE inhibitors—prevents PanIN progression to PDAC induced by diabetes [203]. The gene discussed is KRAS; the disease is Hyperglycemia.