CAAs exhibit a malignant phenotype that is characterized by the increased secretion of leptin, interleukin-6 (IL-6), C-C motif chemokine ligand 2 (CCL2), C-C motif chemokine ligand 5 (CCL5), interleukin-beta (IL-1β), autotaxin (ATX), interleukin-8 (IL-8), vascular endothelial growth factor (VEGF), granulocyte colony-stimulating factor (G-CSF), visfatin and resistin (Figure 2A), which facilitates BC tumor development, progression, and metastasis. Here, CCL2 is linked to neoplasm.