A TGF-β–dominant, CAF-rich, immune-excluded state—scored by high INHBA/periostin/fibronectin, low MHC-I, long CD8+–tumor distances, macrophage/CAF border interfaces, and FBI-like genomic context—would be predicted to benefit from strategies that decompress or reprogram stroma and restore access, including consideration of TGF-β pathway targeting layered onto PD-(L)1 where feasible. Here, TGFB1 is linked to neoplasm.