Though the protein level and transcriptional activities of p53 are maintained at low levels in some cisplatin-resistant tumor cells [36, 37], DNA damage regulated by cisplatin causes an increase in p53 protein stability and consequently impacts cell fate via the raised transcription of p21, which then obstructs cyclin-dependent kinases 1 and 2 (CDK-1 and -2) and causes G1/S and G2/M cell cycle arrest [38]. The gene discussed is CDK1; the disease is neoplasm.