Genomic mutation in the KRAS gene locus results in a continuous activation of the MAPKinase pathway independent from extracellular factors and from the EGFR. Not surprisingly and due to continuous stimulation of the oncogenic signaling pathways by mutatively activated KRAS, inhibition of EGFR had no beneficial or even adverse effects in colorectal cancer patients harboring a KRAS mutation. This evidence concerns the gene KRAS and colorectal cancer.