EPCs by suppression of endothelial cell-specific gene expression in early-stage EPCs and induction of apoptosis in late-stage EPCs. Moreover, CXCL10 and VEGF also play important role in tumor angiogenesis. Our previous study also showed that the downregulation of CXCL10 and VEGF by adiponectin treatment could effectively reduce liver tumor growth and metastasis. Therefore, our result suggested suppression of CXCL10, VEGF, CXCR3 and CXCR4 expression by Tolterodine tartrate FTY720 may be one of the mechanisms contributing to the reduction of circulating EPCs and the decrease of neoangiogenesis. The specific mechanisms of these molecules on FTY720-mediated suppressions of circulating EPCs and neoangiogenesis need to be further clarified. In conclusion, FTY720 suppressed liver tumor metastasis after hepatectomy and I/R Naringin dihydrochalcone injury through attenuating hepatic I/R injury and reducing the numbers of circulating EPCs, suggesting that it may be a promising candidate for potential adjuvant therapies for treating liver cancer metastasis after liver surgery for HCC patients. Genes regulating the hypothalamus-pituitary-adrenal axis are associated with susceptibility to depression as well as antidepressant efficacy. The HPA axis has a wellcharacterized role as a regulator of the neuroendocrine stress response. Its activation leads to the production of glucocorticoids in the adrenal axis, of which the major constituent in humans is cortisol and in rodents is corticosterone. Over the past decade, genome wide association studies for single nucleotide polymorphisms revealed significant associations between susceptibility to depressive episodes and variants in both the NR3C1, that encodes the glucocorticoid receptor, and FKBP5, that encodes a GR binding protein thought to attenuate GR activity. While most studies have focused on the variants in GR because of its role as a transcriptional regulator, the involvement of FKBP5 and its gene product, FKBP51, have received little attention. This is largely due to uncertainty about how to approach this relatively unknown protein. In fact, it remains to be proven whether FKBP51 is a valid therapeutic target for treating depression, despite its clear genetic link. Since the initial discovery of the association between FKBP5 SNPs and depression, other psychiatric disorders have been found to be associated with FKBP5 SNPs including PTSD, bipolar disorder, anxiety, peritraumatic dissociation, and major depression in HIV patients. The TT variant of the rs1360780 SNP was associated with both an increased incidence of depressive episodes throughout a carrier��s lifetime, and increased sensitivity to common neurotransmitter-based anti-depressants. Interestingly, individuals with the rs1360780 TT SNP had significantly higher FKBP51 protein levels in their lymphocytes. FKBP51 levels are also elevated in patients with HIV infection, perhaps playing a role in the depression that commonly occurs with chronic highly active antiretroviral therapies.