Overall, the high-risk subgroup demonstrated larger tumor size, higher pathological grade, enhanced genomic stability, lower mutation rates, and an immunosuppressive TME marked by the presence of myeloid cells-derived cytokines, epithelial-to-mesenchymal transition (EMT), and an enrichment of PI3K-Akt and TGF-β signaling pathways. The gene discussed is AKT1; the disease is neoplasm.