These CAF–tumor interactions are now targeted therapeutically: agents against fibroblast activation protein (FAP) on CAFs (e.g., FAP-specific CAR-T cells or inhibitors) and inhibitors of CAF-derived signals (e.g., TGF-β or IL-6 blockade) are being explored to disrupt the tumor-supportive stroma (66, 68). This evidence concerns the gene TGFB1 and neoplasm.