Our findings on the ability of WIP1 to promote CSC properties and that of a WIP1 inhibitor to suppress these properties in p53-deficient NSCLC cells have defined a new mechanism underlying the therapeutic efficacy of WIP1 inhibitors, and suggest that these inhibitors may have effects beyond p53, and be effective regardless of the p53 status in NSCLC patients with either wild-type or mutant p53. This evidence concerns the gene PPM1D and non-small cell lung carcinoma.