Preclinical researchers reported that interrupting the STING–IL6/STAT3 signaling axis suppressed breast‑cancer bone colonization in experimental models by preventing formation of an osteoclastic niche. The study mapped how tumor‑derived STING activation drives IL‑6 production and downstream STAT3 signaling to remodel bone microenvironments, enabling metastatic growth. Authors propose the axis as a therapeutic target to block bone metastasis; translational work will be needed to identify drug candidates and biomarkers for clinical testing.