It could be shown in tumor bearing patients that exogenous TNF-α administration leads to a corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH) and cortisol release [55], while glucocorticoid administration in healthy subjects suppresses TNF-α production, and the circadian rhythm of endogenous glucocorticoids appears to be inversely correlated with the pro-inflammatory cytokine production [69]. The gene discussed is CRH; the disease is neoplasm.