In recent years, the progress of comprehensive treatment for gastric cancer has significantly lagged behind that of lung cancer, intestinal cancer, breast cancer and other western multi-infarct species. For limited-stage gastric cancer, research focuses mostly on postoperative adjuvant radiotherapy, perioperative radiotherapy and postoperative synchronous radiotherapy. For progressive gastric cancer with poorer prognosis, targeted drugs alone or in combination with targeted drugs, as well as novel chemotherapy regimens have been validated in first- and second-line treatment of gastric cancer. The platinum-based chemotherapy regimen combined with fluorouracil-based drugs has been used in the treatment of gastric cancer for more than 30 years. Although the new generation of platinum-based agents or oral fluorouracil-based agents have proven to be easy to use and moderately well tolerated in recent years, respectively, there has been no significant and substantial improvement in survival time for patients with gastric cancer. The practice of molecularly targeted drug therapy, which has been shown to clearly improve outcomes and prognosis in lung, bowel and breast cancers, can also be difficult in gastric cancer. ToGA is the first large, multicenter, randomized controlled phase III clinical study of trastuzumab in patients with HER2-positive gastric cancer and the first clinical study to demonstrate that chemotherapy combined with a targeted agent improves survival time in progressive gastric cancer. Trastuzumab has now become a new treatment option for patients with HER2-positive progressive gastric cancer. However, the latest longer follow-up results from the ToGA study showed that the survival difference between patients treated with or without targeted agents decreased to 1.4 months from the earliest reported 2.7 months. This suggests that only a small proportion of patients will benefit from the combination of trastuzumab. The publication of the AVAGAST results showed that the anti-angiogenic drug bevacizumab (bevacizumab) did not improve the prognosis of patients with progressive gastric cancer. Apatinib is a small molecule anti-angiogenic tyrosine kinase inhibitor targeting VEGFR, especially VEGFR-2, with independent intellectual property rights in China. Analysis of the results of a phase II clinical trial involving 22 centers showed that Apatinib as a second-line chemotherapy followed by progression-free survival time (PFS) and overall survival time (OS) provided significant benefits. The survival benefit of Apatinib in the treatment of progressive gastric cancer has been further confirmed by an interim analysis of the ongoing Phase III clinical study. Meanwhile, the Phase III clinical trial (REGARD) has again demonstrated that VEGF, a fully human monoclonal antibody acting on VEGFR-2, can be used as a target for gastric cancer treatment. The 119-center international double-blind, multicenter randomized controlled clinical trial enrolled 355 patients with progressive gastric cancer who had received first-line chemotherapy with platinum or fluorouracil-based agents. The results of the study showed that Ramucirumab prolonged patient survival (5.2 months vs. 3.8 months, HR: 0.776, p=0.047). In addition, Ramucirumab increased PFS from 1.3 months to 2.1 months in the control group (p<0.0001) and increased the disease control rate (DCR) from 23% to 49% (p<0.0001). The 49% disease control rate shown in this study has never been achieved in previous clinical studies of progressive gastric cancer treatment. In terms of toxicities, similar to previous studies, the side effects of ramucirumab-targeted therapy were much less severe than those of chemotherapy. < p=""> Ramucirumab was the first targeted agent shown to be effective as a single agent for the treatment of progressive gastric cancer, and the first anti-angiogenic targeted agent shown to improve survival and to result in improved PFS and RR. However, an objective analysis of the study results showed that Ramucirumab resulted in an extension of OS by only 1.4 months and an extension of PFS by only 0.8 months. Most patients had rapid disease progression even after treatment with Ramucirumab. Therefore, the search for molecular markers related to Ramucirumab efficacy and further targeting the superior population are particularly important in the anti-angiogenic treatment of gastric cancer. In recent years, there has been little breakthrough in the molecular markers related to the efficacy of anti-tumor angiogenesis targeted drug therapy. Molecular marker studies targeting AVAGAST have found that levels of circulating VEGF-A and its complex receptor NRP-1 in patients with progressive gastric cancer correlate with the prognosis of receiving bevacizumab in combination with chemotherapy regimens. Patients with higher baseline plasma VEGFR-A levels had a better prognosis than those with lower VEGFR-A levels; while patients with lower baseline plasma NRP-1 levels had a better prognosis than those with higher NRP-1 levels. However, this difference was only statistically significant in the non-Asian population of gastric cancer patients. Meanwhile, the efficacy between single nucleotide polymorphisms (SNPs) in key genes of VEGF and its receptor pathway and anti-angiogenic drug therapy has been screened and validated on a large scale. In a molecular marker study in a clinical trial (AViTA) of patients receiving bevacizumab for pancreatic cancer, the SNP for VEGFR1 (rs9582036) was found to be strongly associated with both overall survival time (HR: 2.1, p=0.00014) and time to disease progression free (HR: 1.89, p=0.00081). In addition, another SNP of VEGFR1 (rs7993418) was shown to be associated with disease-free progression time (HR: 1.81, p=0.033) in renal cancer patients (AVOREN) treated with bevacizumab, but not with overall survival time. And what is the relationship between these SNPs and the prognosis of gastric cancer patients receiving anti-angiogenesis? Are there other efficacy-related molecular markers? In addition, could changes in cellular function resulting from changes in tumor blood supply after anti-angiogenic therapy be a possible marker for the efficacy of anti-angiogenic therapy? We are looking forward to further studies to explore and confirm these questions.