Indeed, certain tumours are notable for their high incidence of activating mutations in KRAS (pancreatic, colorectal and nonsmall cell lung cancer) and BRAF (melanoma, thyroid, hairy cell leukaemia); such cancer cells typically become addicted to these oncoproteins and the hyperactivation of ERK1/2 signalling for proliferation and survival, making the pathway an attractive target for therapeutic intervention. This evidence concerns the gene KRAS and lung cancer.