Thus, KRAS and BRAF oncogenes may function in a mutually exclusive manner in the transformation and carcinogenesis of pancreatic cancers; indeed, some studies suggest that a mutation in one of these two genes invariably results in retention of wild-type copies of the other (Maitra et al., 2006; Koorstra et al., 2008). This evidence concerns the gene KRAS and familial pancreatic carcinoma.