Taken into account that adrenalectomy blocked the increase in TH protein levels in the NTS-A2 during morphine dependence [29], and that a GRE/AP-1 site has been described in the TH gene promoter [53], our data might point out ΔFosB as a mediator in the effects of GC on noradrenergic activity in the NTS-A2 during opiate dependence. The gene discussed is TH; the disease is morphine dependence.