FOXP3 and neoplasm: CAFs have the ability to inhibit T cell proliferation and differentiation and to upregulate expression of PD-L1 on the tumor cells, thus leading to T cell exhaustion, driving polarization of macrophages toward a pro-tumorigenic phenotype (CD163+), and encouraging the influx of T regulatory cells (FOXP3+) and other myeloid-derived suppressor cells.