NNK, a β-adrenergic (β-ARs) agonist, is capable of stimulating DNA synthesis and proliferation of human pancreatic duct epithelial cells lung adenocarcinoma cells via the β-ARs release of arachidonic acid or trans-activation of epidermal growth factor receptor (EGFR) by initiating cAMP signaling [61,62]. This evidence concerns the gene CTBP1 and lung adenocarcinoma.