Nicotine could significantly activate RhoA and increase the expression and enzyme activity of TH in culture rat pheochromocytoma PC 12 cells, and treatment with Y27632 or C3 toxin significantly to block RhoA signaling remarkably inhibited the nicotine-induced increase of TH and catecholamine biosynthesis in PC12 cells (Fukuda et al., 2005), indicating RhoA may be involved in the increase of catecholamine neurotransmitters such as dopamine caused by nicotine and the activation of reward circuits. This evidence concerns the gene TH and pheochromocytoma.