Moreover, F1/F3 treatment augmented the macrophage population while decreasing pro-inflammatory M1 cells and increasing M2 cells (Figure 4A)—an observation that may be attributed to tumor-derived chemokines (e.g., IL-10, CCL2/3/4/5/7/8, CXCL12, VEGF, PDGF, CSF1) that recruit monocytes or M0 macrophages into the TME and induce M2 polarization [41]. The gene discussed is CXCL12; the disease is neoplasm.