TS_FR‒ showed upregulated immune-regulatory and ECM degradation proteins (IL-18, LGALS9, ISG20, and CTSB), along with enriched pathways related to actin cytoskeleton organization, RAC-GTPases, and leukocyte activation, in parallel with FR‒ tumor profiles (Fig. 2e, f), indicating that dysregulated fibroblasts and immune cells may collaborate within the dense stroma in FR‒ tumors. The gene discussed is LGALS9; the disease is neoplasm.