Therefore, if Claspin is overexpressed in radioresistant cells through the deubiquitination action of USP3, the cancer cells can then rely on the activated ATR–Chk1 pathway to overcome the radiation-inflicted damage, either by the repair of damage or by another genome-protective ATR–Chk1-associated action, such as cell cycle arrest and replication fork stability [135]. Here, CHEK1 is linked to cancer.