Lin et al. (2024) have shown that CDK1 is highly overexpressed in endometrial carcinoma, enhancing cell survival, proliferation, invasion, and migration, inhibiting cell apoptosis, and inducing DNA damage dependent on the CDK1-mediated phosphorylation of kinesin family member C1 (KIFC1) and subsequent activation of PI3K/AKT pathway, known to be involved in cell division and proliferation related to tumor development [79]. Here, KIFC1 is linked to neoplasm.