In breast cancer bone metastasis, elevated SOST expression correlates with increased metastasis and poorer survival; silencing SOST reduces cell proliferation and migration, while SOST enhances tumor growth through interactions with STAT3 and TGF-β/KRAS pathways; targeting the SOST-STAT3 interaction with the compound S6 shows promise as a therapeutic strategy to inhibit bone metastasis [39]. This evidence concerns the gene STAT3 and neoplasm.