Collectively, this fibrotic, angiogenic, and metabolically adaptive TME underlies the aggressive clinical course of these subtypes [13] and may support the rationale for therapies targeting the tumor–stroma interface, including TGF-β or fibroblast activation protein-α (FAP) inhibition, ECM modulation, and anti-angiogenic strategies—potentially in combination with chemotherapy or immunotherapy [47,48,49]. This evidence concerns the gene TGFB1 and neoplasm.