This inturn biases mutant KRAS to adopt an “on” confirmation,even in the absence of an extracellular signal, thereby driving aberrantdownstream cellular signaling and tumor formation.1 A majority of KRAS mutations occur at three codon positions(G12, G13, Q61), though mutations at other positions in KRAS alsocan lead to the deregulation of its activity.2 These mutations have a high occurrence in lung,3 colorectal4 and pancreatic cancers.5 This evidence concerns the gene KRAS and familial pancreatic carcinoma.