Consequently, large efforts to analyze the DN effects of tumor-derived p53 mutants on the activation of several target genes have been undertaken in a systematic way using the yeast model, which was able to classify mutations as either dominant or recessive (13), and has also led to the cataloging of p53 mutations based on the ability to regulate a large number of p53-target genes (14). This evidence concerns the gene TP53 and neoplasm.