非酒精性脂肪性肝病（NAFLD）与肥胖、糖尿病、胰岛素抵抗等代谢综合征的关系密切。发病机制目前尚未完全阐明, 治疗上也缺乏有效措施。我们在前期的研究提示GIT2在NAFLD发生中具有重要功能。但是，其作用的分子机制仍不清楚。我们拟通过基因敲除小鼠研究GIT2在NAFLD发生中功能，揭示其在调控TLR信号通路和炎症小体信号通路中的作用分子机制，确定GIT2影响肝脏细胞的类型，分析GIT2在NAFLD等病理组织的表达变化与疾病发生的关系，为NAFLD治疗、新药的靶点设计和病原体感染防治提供新思路。

Nonalcoholic fatty liver disease (NAFLD) is related to obesity, insulin resistance, diabetes and other metabolic syndrome closely. However, the pathogenesis of NAFLD is not yet fully elucidated. We still lack of effective treatment measures. Our results suggest that GIT2 plays a major role in the occurrence of NAFLD. But the molecular mechanisms of GIT2 regulating of NAFLD remain unclear. We will determine the function and molecular mechanisms of GIT2 in the occurrence of NAFLD through GIT2 knockout mice. The molecular mechanisms of GIT2 regulating TLR signaling pathway and inflammasome pathway will be investigated. The liver cell-type that GIT2 regulates will be determined. The expression of GIT2 in the tissue of NAFLD patients and relationship with diseases will be analyzed. We will provide new clues to the treatment of NAFLD, new targets for drug design and prevention of infection of pathogen.