We performed three sets of experiments to test our hypotheses: (i) studies with the HCT116 colon carcinoma cell line and its p21 knockout derivative (HCT116p21−/−); (ii) studies with breast cancer cell lines that differ with respect to TP53 status, and hence constitutive p21 and WIP1 levels; and (iii) studies with the p53 wild-type MCF7 cell line in which WIP1 or p21 was suppressed by pharmacological and siRNA approaches. The gene discussed is PPM1D; the disease is breast carcinoma.