In conclusion, our study revealed that REV1 plays an important role in the generation of radioresistance in lung cancer, that REV1 acts as a scaffolding protein to facilitate Rad18 binding to CTH, and that REV1 promotes CTH ubiquitination and degradation, thereby inducing the formation of an abnormal tumor metabolic microenvironment, which ultimately leads to the development of radioresistance. Here, RAD18 is linked to lung cancer.