ECM‐CAF is enriched at tumour boundary. Notably, its level is significantly higher in non‐responders compared to responders. ECM‐CAF interacts with malignant cells, promoting tumour progression. Additionally, it regulates exhausted CD8+ T cells through immune checkpoint ligand receptors (e.g., LGALS9/TIM‐3), facilitating immune evasion. Here, HAVCR2 is linked to neoplasm.