Although approximately 10% of pancreatic cancers lack KRAS mutations, RAS proteins are activated by receptor tyrosine kinases, including EGFR, which is also required in KrasG12D-driven PDAC.39,84,85 In a recent study, 44% of KRAS wild-type cases exhibited activating mutations in other components of the MAPK pathway, including activating BRAF mutations in approximately 25% of tumors.90 Overall, 3% of PDAC patients have mutations in B-RAF. This evidence concerns the gene KRAS and pancreatic neoplasm.