In this study, our results showed that the anticancer effect of DTX was more effectively enhanced by pKAL in HCT116 colorectal cancer cells (wild-type p53) than in DU145 prostate cancer cells (mutant p53) when wild-type p53 was upregulated by the single treatment of pKAL as well as DTX in HCT116 cells; however, mutant 53 was slightly downregulated by the single treatment of pKAL or DTX in DU145 cells (compare Figure 3a,b and Figure 5a,b). The gene discussed is TP53; the disease is prostate cancer.