Future directions should emphasize selective targeting of pathogenic CAF subsets while preserving tumor‐suppressive populations, disruption of specific CAF–immune cell axes driving resistance (e.g., CXCL12–CXCR4 or TGF‐β signaling), and metabolic reprogramming of CAFs to reverse immunosuppression. The gene discussed is TGFB1; the disease is neoplasm.