By integrating TGF-β–informed readouts (e.g., INHBA+ cancer-associated fibroblast burden, periostin/fibronectin indices, MHC-I status and CD8–tumour distances) with PD-1–based regimens and TGF-β-axis agents (ALK5 inhibitors, Activin A neutralisation, NOX4-directed reprogramming), emerging strategies aim to restore antigen presentation, improve lymphocyte access and remodel tumour–stroma interfaces. The gene discussed is TGFBR1; the disease is neoplasm.