It is unfortunate that so much of the preclinical work on FTIs focused on systems with mutated H-Ras and somewhat surprising that the momentum behind FTIs remained so strong that the large clinical trials went ahead on lung, colon, and pancreatic carcinoma even though it was already clear at that stage that K- and N-Ras could circumvent effective FTase inhibition by an alternative pathway of geranylgeranylation. Here, HRAS is linked to exocrine pancreatic carcinoma.