Mechanistically, the absence of NEIL3 significantly triggered the activation of phosphorylation of the ATR-CHK1 axis, which mitigated DNA damage by initiating the DNA damage response (DDR) pathway, thereby stabilizing replication forks and delaying cell cycle progression, ultimately conferring resistance to radiotherapy or chemotherapy in prostate cancer cells [69,70] (Figure 4). Here, NEIL3 is linked to prostate carcinoma.