KRAS and Obesity: Based on the observation that only a small percentage of mutated Kras is occupied with guanosine triphosphate (GTP) and thus cannot be considered constitutively active [56], Logsdon and colleagues postulated a Ras/Inflammation Feed Forward model, in which oncogenic Kras requires activation by external/inflammatory factors, e.g., as found in obesity, to drive pancreatic neoplasia [57,58].