In order to confirm whether AMPK activity was essential for cell viability after topotecan treatment in cancer cells with wild-type or mutant p53, human colon cancer cells were treated with various concentrations of topotecan in the presence or absence of the AMPK inhibitor, compound C. As shown in Fig. 6, the combined treatment of topotecan with compound C resulted in an increased level of cytotoxicity in human colon cancer cells with wild-type p53 (HCT116 and LS174-T cell lines). The gene discussed is TP53; the disease is cancer.