Osteocytes inhibit tumor development via STING-dependent antitumor immunity. Osteocytes, the most abundant cells in the bone microenvironment, transfer mitochondria to metastatic cancer cells, triggering the cGAS/STING pathway and activating antitumor immunity. This mitochondrial transfer is mediated by Miro1 and MFN2, and its impairment leads to increased bone metastasis progression. Osteocyte mitochondria increase cytosolic mtDNA in cancer cells, activating the cGAS/STING pathway and inducing immune responses. The study reveals that osteocytes play a protective role in bone metastasis by transferring mitochondria to cancer cells, which enhances tumor immunogenicity and antitumor immunity. The findings suggest that targeting mitochondrial transfer between osteocytes and cancer cells could be a therapeutic strategy for preventing bone metastasis. The study also highlights the role of osteocytes in maintaining bone homeostasis and their potential as a target for cancer therapy. The results indicate that intercellular mitochondrial transfer is a universal biological event that occurs in both physiological and pathological conditions, and that osteocytes communicate with cancer cells through this process. The study provides evidence of a new mechanism by which osteocytes inhibit tumor development in the bone marrow microenvironment. The findings have implications for understanding cancer progression and developing new therapeutic strategies for bone metastasis.Osteocytes inhibit tumor development via STING-dependent antitumor immunity. Osteocytes, the most abundant cells in the bone microenvironment, transfer mitochondria to metastatic cancer cells, triggering the cGAS/STING pathway and activating antitumor immunity. This mitochondrial transfer is mediated by Miro1 and MFN2, and its impairment leads to increased bone metastasis progression. Osteocyte mitochondria increase cytosolic mtDNA in cancer cells, activating the cGAS/STING pathway and inducing immune responses. The study reveals that osteocytes play a protective role in bone metastasis by transferring mitochondria to cancer cells, which enhances tumor immunogenicity and antitumor immunity. The findings suggest that targeting mitochondrial transfer between osteocytes and cancer cells could be a therapeutic strategy for preventing bone metastasis. The study also highlights the role of osteocytes in maintaining bone homeostasis and their potential as a target for cancer therapy. The results indicate that intercellular mitochondrial transfer is a universal biological event that occurs in both physiological and pathological conditions, and that osteocytes communicate with cancer cells through this process. The study provides evidence of a new mechanism by which osteocytes inhibit tumor development in the bone marrow microenvironment. The findings have implications for understanding cancer progression and developing new therapeutic strategies for bone metastasis.