From a molecular perspective, YAP may provide a foundation for AR’s oncogenic activity by regulating processes such as cell proliferation and epithelial-mesenchymal transition, while AR may, in turn, enhance YAP’s oncogenic effects through modulation of transcriptional activity.[12,13] The upregulation of YAP and AR in tumor tissues compared to normal controls suggests that these two molecules may jointly contribute to the pathogenesis of osteosarcoma, offering new insights into the molecular mechanisms underlying this disease. This evidence concerns the gene AR and neoplasm.