However, interestingly, in vitro studies showed that neither the presence of oncogenic KRAS nor the level of mutant KRAS activity positively correlated with COX-2 protein levels in pancreatic cancer cells [120,127,128], suggesting that COX-2 overexpression and resultant inflammation might be a critical early event in KRAS hyperactivation during PDAC development. The gene discussed is KRAS; the disease is familial pancreatic carcinoma.