KRAS and pancreatitis: Furthermore, Carrière et al. subjected genetically engineered mice with a Lox-Stop-Lox (LSL) sequence followed by a K-Ras G12D point mutation (LSL-KRASG12D mice) to a series of caerulein injections (previously demonstrated to induce pancreatitis) and found that pancreatitis-induced acinar cell regeneration increased the propensity for pancreatic malignant transformation, confirming the role of inflammation in the development of PanINs and subsequent PDAC [40].