In this regard, it has been firmly established that oncogenic mutations in KRAS behave as one of the earliest stimuli for the formation of PanINs.2, 3 These data are strongly supported by animal models, such as the Pdx1-Cre; LSL-KrasG12D transgenic mice, in which the pancreas-specific expression of oncogenic Kras promotes PanIN occurrence4 and, at a lower frequency, pancreatic cancer. Here, KRAS is linked to familial pancreatic carcinoma.