Uterine leiomyosarcoma (LMS) is recognized as an aggressive form of sarcoma, with certain subsets exhibiting deficiencies in DNA repair mechanisms. Recent research highlights the potential of targeting Polo-like kinase 4 (PLK4) as a therapeutic strategy, particularly in LMS cases characterized by DNA repair defects. Inhibition of PLK4 has been shown to induce chromosome missegregation and increase DNA damage, suggesting that this approach could be effective in treating patients with these specific tumor characteristics (ref: Lee doi.org/10.1158/1078-0432.CCR-23-3720/). Furthermore, the prognostic significance of Stathmin expression has been elucidated, with findings indicating that higher levels correlate with increased mitotic counts, atypia, and vascular invasion. In survival analyses involving 165 patients, Stathmin emerged as a critical independent prognostic marker, alongside age and FIGO stage, emphasizing its role in predicting disease-specific survival (ref: Davidson doi.org/10.1097/PGP.0000000000001030/). Additionally, a novel nomogram has been developed to assess the risk of special uterine leiomyoma pathological types or leiomyosarcoma in postmenopausal women, providing a valuable tool for early detection and intervention (ref: Wang doi.org/10.2147/RMHP.S461773/).