Indeed, activation of MAPK signaling (but not PI-3K/AKT) recapitulated the effects of activated KRAS in mice, supporting the role of MAPK as an essential effector of KRAS in PDAC.33,34 Indeed, our group has also demonstrated MAPK-dependent pancreatic cancer growth;3,4 and targeting MAPK should reasonably lead to cytotoxic outcomes. This evidence concerns the gene KRAS and familial pancreatic carcinoma.