KRAS mutation leads to constitutive K-Ras activity in association with stimulated autocrine production of the EGFR ligand as reported in panc-1 pancreatic carcinoma cells [9], A549 lung cancer cells and MDA-MB-231 breast cancer cells [10], [11] as well as in CRC cell lines LIM1215, OXCO-2 and DiFi that develop resistance to cetuximab, presumably due to a secondary KRAS mutation[12] (Fig. 1). This evidence concerns the gene KRAS and exocrine pancreatic carcinoma.