Although nicotine is not a conventional carcinogen, this tobacco smoke-related compound has been shown to induce the secretion of growth factors (such as bFGF, TGF-α, calpains, and VEGF), resulting in the activation of Raf, Akt or PKC pathways for the growth promotion of lung epithelial or cancer cells and upregulation of Bcl-2 signaling that is responsible for the increase in the resistance to anti-cancer therapies [35,36]. This evidence concerns the gene BCL2 and cancer.