TGFB1 and chronic pancreatitis: Interestingly, murine pre-neoplastic pancreatic epithelial cells with mutant KRAS transiently exposed to exogenous TGFβ1, i.e., corresponding in vivo to pulses of TGFβ1 produced during chronic pancreatitis, a known risk factor for PDAC [54], converted to a partially mesenchymal (PM), progenitor-like, and hyper-proliferative state in vitro, which was stable and maintained by aTGFβ [27].