It was shown that TAMs might release CCL2, which induced MCF10A to develop an EMT and an invasive phenotype by increasing endoplasmic reticulum oxidoreductase-1 (ERO-1) and matrix metalloproteinase-9 (MMP9).318 Similarly, TAM-secreted CCL5 may significantly increase prostate cancer cell invasion, metastasis, and EMT through activation of the β-catenin/STAT3 signaling pathway.319 With the help of CCL5 binding to CCR5 in macrophages, malignant phyllodes tumor could attract and repolarize TAMs, activating the AKT signaling pathway. The gene discussed is STAT3; the disease is cancer.