Lung cancer is the leading cause of cancer-related deaths worldwide. Despite therapeutic advances over the last several decades, the overall 5-year survival remains only 16%. (Siegel R, 2013). Molecular studies have indicated that Adenocarcinomas have distinct genomic alterations allowing classification into clinically relevant molecular subsets. Such specific molecular level alterations are sometimes important for initiation and maintenance of the tumour serving as “drivers” in lung cancer tumorigenesis. Not only is mutant KRAS difficult to restrain, its presence in some types of cancers predicts that there will be no response to other targeted drugs. For example, patients with colorectal cancer may benefit from additional treatment with an antibody drug that targets the EGFR protein (cetuximab or panitumumab). However, this benefit is seen only in patients who have a “wild-type” (not mutated) KRAS gene. The reason for this is that EGFR and other related receptor proteins rely on KRAS to transmit proliferation signals.