A high-fat diet was able to ameliorate mutated KRAS activity, increasing fibrosis and enhancing PDAC progression in a mouse model [121], and a recent study with an in vivo mouse model showed a causal and positive correlation between obesity and early PDAC progression, identifying altered beta cell expression of cholecystokinin (Cck) in response to obesity and defining islet Cck as a promoter in oncogenic KRAS-driven PDAC [122]. The gene discussed is CCK; the disease is obesity disorder.