Hepatic NK cells preserve breast cancer dormancy via IFN-γ signaling, whereas the CXCL12‒CXCR4 axis-mediated crosstalk imbalance between hepatic stellate cells and NK cells destabilizes tumor quiescence.31 In the epidermal layer, tissue-resident memory T cells enforce melanoma dormancy through dynamic immune surveillance.87,88 Collectively, these findings reveal that tumor dormancy fundamentally represents a spatially orchestrated dynamic equilibrium established through molecular dialogs within niche microenvironments. The gene discussed is CXCL12; the disease is neoplasm.