Further evidence for the role of nicotine-mediated induction of an autocrine catecholamine loop resulting in enhanced proliferation of pancreatic tumors was obtained in a mouse xenograft model where it was found that mice treated with nicotine had increased circulating levels of the catecholamines—adrenaline and noradrenaline—as well as systemic cAMP, which coincided with increased xenograft size and increased protein levels of cAMP, p-ERK1/2, and p-CREB [54]. The gene discussed is CREB1; the disease is pancreatic neoplasm.