In A549 lung carcinoma cells, ROS level elevation caused by nicotine treatment resulted in the phosphorylation of Akt and ERK kinases and to the stabilization of hypoxia-inducible factor 1α (HIF-1α) (Guo et al. 2012), whereas in HepG2 hepatocytes, nicotine treatment was shown to activate the NF-κB response element (Crowley-Weber et al. 2003). The gene discussed is HIF1A; the disease is lung carcinoma.