It has been known for some time that TGFβ-induced EMT of pancreatic carcinoma cells is dependent on activation of RAS/RAF/MEK/ERK signaling [14], but even activation of RAS alone can have an effect on EMT: The introduction of oncogenic K-RAS (V12) in primary pancreatic duct epithelial cells not only drives cell cycle progression and cell growth, but also leads to loss of E-cadherin and gain of N-cadherin expression [50]. This evidence concerns the gene KRAS and exocrine pancreatic carcinoma.