Under clozapine treatment, with the maximum control over drug compliance, and receiving the same amounts of daily diet and exercise. Alongside these strengths, however, we would be remiss in not noting some marked limitations to this study. First, the size of our sample is small, especially for the purposes of sex AbMole GSK 650394 stratification, and accordingly our findings should be viewed as preliminary until replicated and independently verified. Second, our subjects are 
chronic patients, and other AAP treatment prior to this study may have already influenced the risk for MetS, lessening the effects attributable to clozapine that the patients are currently being treated with. Third, patients’ baseline metabolic parameters prior to clozapine treatment and their previous antipsychotic agents were unknown, which may potentially confound the results obtained in this study. Lastly, the ideal pharmacogenetic study design is a longitudinal, prospective, randomized and parallelcontrol clinical trial. However, our study was cross-sectionally designed rather than longitudinally, therefore we cannot affirm that some subjects in the non-MetS group did not develop MS after the investigation. To avoid the negative consequences of this potential bias, it is important to replicate this data using larger studies that are better designed to find conclusive and not simply suggestive evidence of the associations that we noted in the present study. In summary, in this study we tested for the first time the relationship between the BDNF Val66Met polymorphism and MetS in patients with schizophrenia under long-term clozapine treatment. We concluded that BDNF appears to have a weak association with clozapine-induced MetS, and this effect is only evident in male patients. Large-scale longitudinal studies should be conducted to replicate these findings and offer more conclusive evidence. An important physiological function of these cells is their ability to eliminate and detoxify microorganisms, endotoxins, degenerated cells, immune complexes, and toxic agents. Therefore, KCs play an important role in liver physiological homeostasis and are intimately involved in the liver’s response to infection, toxins, transient ischemia, and various other stresses through the expression and secretion of soluble inflammatory mediators. KCs can be classically activated or alternatively activated. M1 macrophages are associated with the proinflammatory response and produce associated cytokines such as IL-1b, IL12, IL-23, and TNF-a. M2 macrophages are associated with downregulation of immune responses and IL-10 production. Cytokines act as protective mediators for recovery of normal liver function, however, in some instances, excessive activation of KCs may result in exacerbation of the damage. Proper therapeutic modulation of the inflammatory activities of KCs provides opportunities for new treatment approaches toward liver disease.