The primary source of EMT-activating IL-6 within the breast metastatic niche appears to be the mature adipocytes, which secrete IL-6 and stimulate STAT3 signaling in tumor epithelial cells to trigger EMT response, including enhanced cell migration and invasion downstream of IL-6/STAT3-stimulated lysyl hydroxylase-2 (LH2) and tropomyosin receptor kinase B (TrkB) expression [87,88,89]. Here, STAT3 is linked to neoplasm.