Since p53s bind to p300 via their N-terminal domains (Gu and Roeder, 1997) that are intact in the p53LCs, these results indicate that p53-393*78 and p53-374*48 are not accessible to acetylation-mediated activation and thus provide another mechanism underlying the LOF and DN phenotypes of p53LCs in cancer cells, though it remains to be found how exactly p53LCs fail to bind to their target promoters and how to be good substrates for p300. This evidence concerns the gene TP53 and cancer.