Additionally, it has been reported that cancer cells can exit mitosis prematurely through slow degradation of Cyclin B, ultimately leading to drug resistance.49 CDC6 knockout significantly reduced the expression of p-CDK1 and upregulated Cyclin B, both of which are essential for mitotic exit through separase.34 Taken together, these findings suggest that targeting CDC6 may represent a promising strategy for enhancing the therapeutic efficacy of paclitaxel. Here, CDK1 is linked to cancer.