TIGIT, a newly identified immune checkpoint, is highly expressed on various immune cells, including CD8+ T cells, CD4+ T cells, NK cells, and Tregs. It plays a role in NK cell exhaustion and T cell exhaustion, and its primary ligand, CD155, is a potential target for immunotherapy. Anti-TIGIT therapy, either alone or in combination with anti-PD-1 agents, has shown promise in preclinical studies but has faced challenges in clinical trials. For example, the TIGIT-targeted antibody tiragolumab failed in two new trials for advanced lung cancer. TIGIT is involved in immune suppression through interactions with CD155, CD112, and CD112R, and its expression is influenced by various factors, including IFN-I, chemotherapy, and hypoxia. TIGIT is also involved in the regulation of T cell and NK cell function, and its expression is associated with tumor progression and patient outcomes. Preclinical studies have shown that anti-TIGIT therapy can enhance immune cell activation and improve antitumor responses. Clinical trials of anti-TIGIT agents, including tiragolumab, vibostolimab, domvanalimab, and ociperlimab, have shown mixed results, with some trials demonstrating improved outcomes in certain patient populations. However, the effectiveness of TIGIT-targeted therapy may depend on the expression of TIGIT and other biomarkers, as well as the tumor microenvironment. Future research is needed to better understand the role of TIGIT in cancer immunotherapy and to develop more effective treatment strategies.TIGIT, a newly identified immune checkpoint, is highly expressed on various immune cells, including CD8+ T cells, CD4+ T cells, NK cells, and Tregs. It plays a role in NK cell exhaustion and T cell exhaustion, and its primary ligand, CD155, is a potential target for immunotherapy. Anti-TIGIT therapy, either alone or in combination with anti-PD-1 agents, has shown promise in preclinical studies but has faced challenges in clinical trials. For example, the TIGIT-targeted antibody tiragolumab failed in two new trials for advanced lung cancer. TIGIT is involved in immune suppression through interactions with CD155, CD112, and CD112R, and its expression is influenced by various factors, including IFN-I, chemotherapy, and hypoxia. TIGIT is also involved in the regulation of T cell and NK cell function, and its expression is associated with tumor progression and patient outcomes. Preclinical studies have shown that anti-TIGIT therapy can enhance immune cell activation and improve antitumor responses. Clinical trials of anti-TIGIT agents, including tiragolumab, vibostolimab, domvanalimab, and ociperlimab, have shown mixed results, with some trials demonstrating improved outcomes in certain patient populations. However, the effectiveness of TIGIT-targeted therapy may depend on the expression of TIGIT and other biomarkers, as well as the tumor microenvironment. Future research is needed to better understand the role of TIGIT in cancer immunotherapy and to develop more effective treatment strategies.