The 21kD guanine-nucleotide binding proteins (K-Ras, H-Ras, and N-Ras) cycle between active (GTP-bound) and inactive (GDP-bound) forms (1). Receptor tyrosine kinases and G-protein coupled receptors activate Ras, which then stimulates the Raf-MEK-MAPK pathway (2-4). GTPase-activating proteins (GAP) normally facilitate the inactivation of Ras, however in 30% of human tumors point mutations in Ras prevent the GAP-mediated switching off of this pathway (5). The most common oncogenic Ras mutation found in tumors is Glycine 12 to Aspartate (G12D), which prevents Ras inactivation possibly by increasing the overall rigidity of the protein (5,6).