Using in- vitro experiments with mouse embryonic fibroblasts (MEFs) and human cancer cells harboring p53E224D, and in-vivo experiments with genetically engineered mice, we find that the p53E224D point mutation loses the ability to suppress tumor development because it causes a loss of p53 function as a result of mis-splicing of the p53 mRNA transcript. This evidence concerns the gene TP53 and neoplasm.