One proposed mechanism underlying the accumulation of Treg following RT is the enhanced secretion of TGF‐β1 and TGF‐β2 by irradiated tumor cells [174], another potential mechanism may be that RT‐induced CCL2 expression in tumor cells promotes the CCR2‐dependent recruitment of TNFα‐producing monocytes and CCR2+ Treg cells, whose crosstalk via TNF‐α signaling leads to Treg activation and attenuates the antitumor efficacy of RT [175].Compared with nonirradiated tumors, TIL‐Treg from irradiated tumors exhibit similar or even greater suppressive capacity. This evidence concerns the gene CCL2 and neoplasm.