Recent studies have elucidated the genetic and molecular underpinnings of endometrial cancer, particularly focusing on the roles of chromatin remodeling and key genetic mutations. One significant finding is the role of the mSWI/SNF family of chromatin remodelers, where deficiencies in ARID1A and ARID1B lead to the loss of canonical BAF complexes, resulting in increased abundance of noncanonical BAF and PBAF complexes. This shift is associated with the maintenance of the oncogenic state in dedifferentiated endometrial carcinomas, highlighting potential therapeutic targets (ref: St Laurent doi.org/10.1038/s41588-025-02333-9/). Additionally, the loss of PTEN, a common alteration in endometrial cancer, enhances PI3K/AKT signaling, promoting cellular proliferation and resistance to apoptosis, which is critical for tumor progression (ref: Vidal-Sabanés doi.org/10.1038/s41419-025-08022-z/). The genomic landscape of endometrial polyps has also been explored, revealing recurrent mutations in UBE2A, suggesting its role as a novel driver gene in tumorigenesis (ref: Reinikka doi.org/10.1186/s13073-025-01556-z/). Furthermore, a radiomics-based prognostic model has been developed to predict progestin resistance in fertility-preserving endometrial cancer patients, indicating the potential of non-invasive imaging techniques in treatment planning (ref: Li doi.org/10.1097/JS9.0000000000003629/). The ENDORISK-2 model integrates molecular classification and myometrial invasion assessment to improve preoperative risk stratification, demonstrating the importance of personalized approaches in managing endometrial cancer (ref: Lombaers doi.org/10.1016/j.ejca.2025.116058/).