To further interrogate the p53-dependency of the CST5 expression, the colorectal cancer cell lines HCT116 and RKO and their isogenic p53-deficient variants, which were generated by homologous recombination [39], were treated with either nutlin-3a, a small-molecule inhibitor of MDM2 [40], or the DNA-damaging agent etoposide (Figure 2). The gene discussed is CST5; the disease is colorectal cancer.