Importantly, out studies have shown that COX-2 ablation dramatically inhibited the synergistic interaction between HFD and mutant KRAS in enhancing aerobic glycolysis and pancreatic tumorigenesis, indicating that targeted inhibition of COX-2 might be an effective intervention strategy for the suppression of oncogenic KRAS-driven pancreatic cancer metabolism in obese patients. Here, KRAS is linked to pancreatic neoplasm.