Under UV irradiation, MRS is phosphorylated at Ser662, which induces the release and nuclear translocation of AIMP3, thereby facilitating DNA damage repair (Kwon et al., 2011); 2.MRS stabilizes CDK4 (cyclin-dependent kinase4), promotes G1-to-S cell cycle transition, and enhances the tumorigenic ability of cancer cells, and this effect is much more obvious in cancers that are deficient in p16INK4a, which blocks the function of CDK4, thereby suppressing cell cycling (Musgrove et al., 2011; Kwon et al., 2018). This evidence concerns the gene CDKN2A and cancer.