Therefore, in order to distinguish whether the observed differential drug responses were indeed related to p53, or rather were an expression of the general genetic heterogeneity of these aneuploid tumor cells, we used an HCT116 colon carcinoma cell line where the p53 gene (or one of its crucial target genes, the cyclin-dependent kinase inhibitor p21Waf1, which was found to mediate p53's repression of survivin [40]) was disrupted by targeted homologous recombination [41,42]. This evidence concerns the gene BIRC5 and neoplasm.