The suppressive function and phenotype of Tregs strongly depends on TGF-β signaling. One might speculate that TGF-β is also involved in the DNA damage response of irradiated Tregs, as it is well documented that canonical TGF-β signaling played an important role in protecting cells from γ-irradiation by decreasing DNA damage and reducing apoptosis [91]. Wu et al. showed that inhibition of TGF-β1 enhanced the radiation therapy-induced cell death in prostate cancer and this effect was associated with attenuated nuclear accumulation of p-ATM and subsequently increased DNA damage [92]. Another mechanism by which TGF-β1 regulates DNA damage response is by facilitating the non-homologous end joining repair process upon γ-irradiation by upregulating Lig4 [93].