TEA转录因子4（TEAD4）是Hippo信号通路中转录共激活子YAP/TAZ下游最重要的转录因子TEAD家族的成员之 一。近年来，TEAD4的促癌作用被逐渐发现，其可与YAP形成转录复合体或不依赖于YAP独立调控下游相关靶基因的表达， 在 胃肠道肿瘤、肝癌、肺癌、乳腺癌等多种人类实体肿瘤中发挥促癌作用，导致肿瘤的发生和进展，并且是多种肿瘤不良预后的标 志。此外，靶向TEAD4及以阻断YAP-TEAD4结合为靶点的药物在多种肿瘤的体外实验及动物模型中取得显著的治疗效果， 提 示TEAD4可能是肿瘤治疗的一个理想靶点。本文就目前TEAD4在肿瘤发生、发展及治疗中的研究现状作一总结及展望，以期 为TEAD4的后续研究及以其为靶点的肿瘤治疗提供新思路。

Objective Rheumatoid arthritis (RA) is a systemic autoimmune disease, which mainly involves joints across the body, resulting in joint stiffness and loss of daily activity. Recent evidence suggests that numerous self-reacting T cells, including Th1 and Th17, infiltrate the synovium in RA patients, accompanied by functionally-compromised Treg. Iguratimod, a new small molecule with anti-inflammatory and immunomodulatory effects, has shown curative effects in animal models of arthritis. In this study, we aimed to test the clinical effects of Iguratimodˊs on RA patients and its role in immunoregulation. Methods We examined the clinical effects of iguratimod on RA patients in a random controlled clinical trials and analyzed its effects on Th1, Th17 and Treg as well as their associated cytokines and transcription factors by flow cytometry and real-time polymerase chain reaction (PCR). Then t-test, chi-square test and rank sum test were used to conduct statistical analysis. Results Our results revealed that iguratimod therapy provided significantly greater clinical benefit [ACR20, ACR50, ACR70 reached 50%, 20%, 15% respectively in iguratimod treatment group, Z=-2.216,P=0.027] than placebo group with the reduction of Th1 and Th17 but increment of Treg after iguratimod treatment [Th1: week 0 (26.5 ±8.0)%, week 24 (14.2 ±7.3)%, P<0.01; Th17:week 0 (1.7±0.7)%, week 24 (1.3±0.4)%, P<0.05;Treg:week 0 (6.8±1.6)%, week 24 (8.9±2.9)%, P<0.05], which was statistically significant. Conclusion Our results provide theoretical and clinical based evidence for the impact of iguratimod on immunomodulation of RA.