Notably, rosiglitazone, a PPARγ agonist, can partially decrease C–C motif chemokine ligand 2 (CCL2) secretion by tumour cells and reduce the infiltration of TAMs to the irradiated tumour site, thereby delaying tumour regrowth after radiotherapy, suggesting that the combination of the PPARγ agonist rosiglitazone with radiotherapy can enhance the effectiveness of radiotherapy [111]. Here, CCL2 is linked to neoplasm.