Multi-omics analyses have demonstrated that COL11A1+ CAFs are enriched at the tumor margins of ICI-nonresponsive NSCLC, where they impede contact between tumor cells and cytotoxic T lymphocytes and cooperate with SPP1+macrophages to promote immune resistance (53).In another study, abundant infiltration of antigen-presenting CAFs (apCAFs) within the TME was shown to induce Treg proliferation, thereby establishing a highly suppressive immune-resistant milieu (64). Here, COL11A1 is linked to neoplasm.