Additionally, TP53 mutations, although infrequent in MA, have been shown to predict SO development and correlate with aggressive clinical behavior (10) A study has demonstrated that high-grade adenosarcomas exhibited molecular heterogeneity, characterized by genomic instability and TP53 mutations; and BAP1 inactivation appeared to be a specific pathogenic driver in a subset of adenosarcomas (9). This evidence concerns the gene TP53 and adenosarcoma.