This, in turn, upregulates the expression of pro-angiogenic genes (VEGF), increases immunosuppressive and tissue remodeling cytokines (IL-10, transforming growth factor-beta (TGF-β)), suppresses pre-activated T cell proliferation, enhances recruitment and proliferation of Tregs and other immunotolerant myeloid lineages (macrophage colony-stimulating factor (M-CSF), CCL2), promotes Th2 differentiation while suppressing Th1 responses (PGE2), and decreases cancer neo-antigen expression by APCs [118,119,120,121,122,123]. The gene discussed is CCL2; the disease is cancer.