Taken together, these results further confirmed the findings that ANTXR1 plays a crucial role in regulation of TME in GC, which functions by driving the recruitment of immunosuppressive cells to secrete soluble factors, modulating M2 and CAF transformation, mediating T cell exhaustion, and prompting EMT; this can ultimately motivate tumor immune evasion, leading to adverse clinical outcomes for GC patients. This evidence concerns the gene ANTXR1 and neoplasm.