The contribution of CRF to withdrawal-related anxiety is supported by findings that agents which interfere with the normal actions of CRF (i.e., CRF antagonists) can reduce the anxiety if they are administered into the blood (i.e., systemically) (Breese et al. 2005; Sommer et al. 2008) or directly into the CNS—that is, either into the fluid-filled spaces of the brain (i.e., brain ventricles) (Baldwin et al. 1991; Valdez et al. 2003) or into the central nucleus of the amygdala (Rassnick et al. 1993). The gene discussed is CRH; the disease is Anxiety.