Recent research has highlighted the complex biological mechanisms underlying endometrial cancer (EC), particularly focusing on the role of protein arginine methyltransferase 3 (PRMT3) in malignant progression and treatment resistance. A study utilizing data from the Cancer Genome Atlas and Clinical Proteomic Tumor Analysis Consortium databases found that PRMT3 inhibition significantly enhances the susceptibility of EC cells to ferroptosis, suggesting a potential therapeutic target for improving treatment outcomes (ref: Wang doi.org/10.1002/advs.202303812/). Additionally, the SIENDO trial has provided insights into the efficacy of selinexor in patients with TP53 wild-type advanced/recurrent EC, indicating a shift in therapeutic strategies for this challenging cohort (ref: Gouda doi.org/10.1016/j.medj.2023.10.005/). Furthermore, a nomogram predictive model was developed to assess recurrence risk in EC patients, demonstrating good discriminative power and offering a valuable tool for clinical decision-making (ref: Miao doi.org/10.3389/fendo.2023.1156169/). These findings collectively underscore the need for continued exploration of molecular targets and predictive models to enhance the management of EC. Contradictory findings regarding the role of aberrant β-catenin distribution in predicting recurrence highlight the complexity of tumor biology, as it did not correlate with recurrence in a recent study (ref: Beshar doi.org/10.1016/j.ygyno.2023.10.025/).