A study in Science Bulletin reported how macrophages contribute to resistance to immune checkpoint blockade in gastric cancer, identifying immune checkpoint therapy as effective only for subsets of patients. Researchers linked tumor-associated macrophage programs to weakened antitumor immunity, providing mechanistic targets for combination strategies. In parallel, research published in Nature Communications connected neutrophil extracellular traps (NETs) to liver metastasis by disrupting NK cell surveillance through CCDC25. The findings expand the map of immune evasion across organs, linking innate immune extracellular defense mechanisms with metastatic capability. These two updates illustrate an immunotherapy-resistant reality in solid tumors: failure modes can arise from both suppressive myeloid cells and innate immune structural traps that shift the tumor microenvironment away from effective tumor clearance. For drug developers, the actionable angle is clearer immune-pathway targeting—either by reprogramming myeloid cells or by interrupting NET-driven loss of NK function—alongside checkpoint blockade.