Furtherly, it has been reported that CDK1-mediated p53 phosphorylation at ser315 negatively regulate p53 stability and function [47], and that cervical carcinoma cells became more susceptible to camptothecin, an anti-tumor agent, when cyclin B1, the regulatory subunit of CDK1, was silenced. The gene discussed is TP53; the disease is cervical carcinoma.