By regulating the Sipeimine expression of chemokines and/or their receptors. MCP-1 and its receptor CCR2, as well as CX3CL1 and its receptor CX3CR1, were reduced in the atorvastatin-treated group. CCR2 is expressed on the majority of blood monocytes, other leukocytes, and a subset of T cells, mainly responding to directed cell migration toward its primary ligand MCP1. In addition, CCR2-deficient animals ex decreased susceptibility to atherosclerosis and decreased intimal hyperplasia following arterial injury. Similarly, CX3CR1 is expressed on monocytes, natural killer cells, a subset of T cells, and SMCs. Its ligand CX3CL1, a membrane-bound chemokine, is increased in atherosclerosis. The ability of this molecular pair to mediate leukocyte adhesion and migration under physiological flow conditions in vitro was first reported in 1998. A recent study showed that CX3CR1-deficient mice exhibit impaired macrophage and dendritic cell accumulation during vascular inflammation and are protected from intimal hyperplasia in an arterial injury model. In conclusion, 10 mg/kg/d atorvastatin treatment inhibited unstable plaque development in ApoE-deficient mice independent of plasma cholesterol levels. The beneficial effect of atorvastatin is achieved via the inhibition of macrophage infiltration due to the modulated expression of chemokines and their receptors. Mammalian target of rapamycin, also known as FRAP, was originally discovered about 15 years ago in the study on the mechanism of action of rapamycin. mTOR, a conserved serine/threonine kinase, has been recognized as a central regulator of vital cellular processes through PI3K/AKT/mTOR pathway, such as proliferation, growth, differentiation, survival, and angiogenesis by controlling mRNA translation, ribosome biogenesis, autophagy, and metabolism. In human, this pathway is frequently activated in many human diseases, including cancers, furthermore, and uncontrolled mTOR signaling had been reported to be associated with poor clinical outcome in lung, cervical, ovarian and esophageal cancers. In light of the critical role of mTOR in maintaining proper cellular functions, it is biologically plausible that genetic variations in this gene may affect cancer risk and clinical outcome of cancer patients. Recently, a number of case-control studies reported that the polymorphisms in mTOR gene were associated with individual��s susceptibility to cancer risk and clinical outcome, but these studies were limited to modest sample size, Ergosterol different ethnicity, and statistical power. Therefore, we carried out a meta-analysis on all eligible studies to estimate the association between the genetic polymorphisms in mTOR gene and overall cancer risk as well as clinical outcomes. After reviewing literature, we found that besides rs2295080 and rs2536, another polymorphism rs11121704 in intron, have been mostly frequently studied, thus, were included in our meta-analysis. This meta-analysis examined the association between the common genetic polymorphisms and cancer risks as well as clinical outcomes. A total of 5798 cancer patients and 6244 controls were included for cancer risk assessment and 1928 cancer patients were included for clinical outcome assessment.