Activating mutations of KRAS that lead to aberrantsignaling and hyperactivation within the MAPK pathway are among themost common driver mutations in human cancers.1,2 These KRAS mutations, a majority of which are single codon mutations(G12, G13, Q61, etc.), show a high occurrence in some of the mostaggressive cancer types: non-small-cell lung cancer (NSCLC), colorectalcancer (CRC), and pancreatic cancers.1,2 The prevalenceof KRAS mutations has made KRAS a prime target foroncology drug discovery programs for several decades. This evidence concerns the gene KRAS and familial pancreatic carcinoma.