KRAS and pancreatic ductal adenocarcinoma: For example, in pancreatic ductal adenocarcinomas that are strictly dependent on Kras mutations, mutated Kras caused a 1.2–1.5 fold increase in glucose consumption and a 1.3–1.4 fold increase in lactate production that was sufficient to increase hexosamine and nucleotide synthesis that contributed to anabolic metabolism [47].