Evidence suggests that hypothalamus-pituitary-adrenal (HPA) axis imbalance and inflammation such as increased interleukin-1 (IL-1), IL-6, and tumor necrosis factor alpha (TNF-α) cytokine secretion play a crucial role in the etiology of tumors [1, 2]. Dysregulation of the HPA axis has been observed in patients with cancer [3, 4]. Attributed to the participation of corticotrophin-releasing hormone (CRH) in both HPA and inflammation, there is a strong link between CRH and tumorigenesis development (Chap. 1 ). As reported, CRH-like immunoreactivity can be found in tumors composed of peptide-hormone-producing endocrine cells [5]. The peripheral biosynthesis of CRH has also been demonstrated in a large variety of human cancer cell lines, such as neuroblastomas, small-cell lung cancers, and melanomas [6, 7]. However, the effects of CRH on tumor are complicated because of the absence of an absolute clear-cut between the central and peripheral effects of CRH on inflammation and cancer. Until now, little is known about the direct relationship between central CRH and tumorigenesis. In addition to CRH, other corticotropin-releasing hormone (factor) family peptides (CRF peptides, CRFp), including CRH, urocortin (UCN1), urocortin 2 (UCN2), urocortin 3 (UCN3), and CRF binding protein (CRF-BP), as well as their corresponding receptors (CRFr, including CRF1 and CRF2), are found to be involved in tumors [8, 9].