These CAAs facilitate tumour angiogenesis and epithelial changes through secreting chemokines, such as chemokine (C–C motif) ligand 5 (CCL5) and chemokine (C–C motif) ligand 2 (CCL2), alongside with inflammatory mediators including IL-6 and TNF-α, which push BC cells towards a more aggressive phenotype [65] (Fig. 3). The gene discussed is CCL2; the disease is neoplasm.