Although nicotine is not regarded as a carcinogen [7], it may contribute to the pathogenesis of LC, by binding nicotine-derived NNK to the homomeric α7 nicotinic acetylcholine receptor (α7nAChR), which results in significantly activated of α7nAChR-mediated cellular signaling pathways [8,9]. The gene discussed is CHRNA7; the disease is laryngotracheoesophageal cleft.