The regulation of cell proliferation by CLR4CDT2 ubiquitin ligase was due to the degradation of its important substrates, such as CDT1, p21, and SET8. The depletion of CLR4CDT2 led to the accumulation of CDT1 and MLN4924 induced apoptotic death was partially rescued by the depletion of CDT1, indicating a role to CDT1 as a possible target in ovarian cancer development and treatment (Pan et al., 2013; Wu et al., 2021). This evidence concerns the gene KMT5A and ovarian cancer.