Oncogenic mutations in KRAS protein, presented in approximately 90% of pancreatic cancers, 45% of colon cancers, and 35% of lung cancers, impair GAP-stimulated GTP hydrolysis activity, which hampers the protein in switching between active and inactive states, rendering RAS in constitutively active GTP-bound status [2,10,11] (Figure 1). Here, KRAS is linked to familial pancreatic carcinoma.