More recently, in a murine model of bladder cancer, radiotherapy induced the release of CCL2 by irradiated cancer cells, which in turn, promoted the recruitment of bone marrow-derived CCR2-positive myeloid cells and the polarization of M1-type TAMs toward the M2 type, suggesting a radio-resistance mechanism sustained by a CCL2-M2 macrophage network [39]. The gene discussed is CCL2; the disease is urinary bladder cancer.