Correspondingly, depletion of perivascular NG2+ Nestin+ MSCs or disruption of TGF-β2 signaling disrupts quiescence, triggering bone metastasis recurrence.84 Similarly, a recent study indicated that alveolar macrophages sustain the suppression of breast cancer pulmonary metastasis via persistent TGF-β2–TGFβRIII interplay, while signal inactivation precipitates dormancy escape.85 Age-dependent microenvironmental alterations profoundly influence dormancy regulation. The gene discussed is TGFB2; the disease is breast cancer.