Although the mutation did not affect the ATF3–p53 interaction (Fig. 6d), nor its nuclear localization (Fig. 6f), R88G failed to increase the p53 level (Fig. 6e, lane 4 vs. lane 3), nor promote p53 to transactive its responsive promoter (Fig. 6g, lane 4 vs. lane 3), indicating that this cancer-derived, ubiquitination-devoid mutant lost the ability to activate p53. This evidence concerns the gene ATF3 and cancer.