Based on this, intervention strategies present a bidirectional approach—inhibition of pro-tumour factors (e.g. IL-6 monoclonal antibody) or activation of anti-tumour signals (e.g. upregulation of CXCL10 by HDAC3 inhibitors) can both remodel the TME ecology, whereas targeting the TGF-β-mediated fibrotic process (e.g. Galunisertib) also reduces microenvironmental stiffness to reverse mechanical stress-driven YAP/TAZ activation and achieve multidimensional anti-tumour effects [59, 60, 71]. Here, CXCL10 is linked to neoplasm.