Recent research has significantly advanced our understanding of the molecular mechanisms and genetic alterations associated with endometrial carcinoma (EC). A comprehensive study characterized a cohort of 138 tumors and 20 normal tissues using ten different omics platforms, revealing that targeted quantitation of specific peptides could predict the activity of antigen processing and presentation machinery, potentially guiding immunotherapy selection (ref: Dou doi.org/10.1016/j.ccell.2023.07.007/). Another study involving multi-omic profiling of 687 tumors identified aberrant DNA methylation patterns that correlate with changes in RNA and protein abundance, contributing to a Pan-Cancer catalog that includes endometrial tumors (ref: Liang doi.org/10.1016/j.ccell.2023.07.013/). Furthermore, functional analyses have demonstrated that Trp53 mutations exhibit varying phenotypic effects, with missense mutations being stronger drivers of carcinogenesis compared to deletions, while Fbxw7 mutations alone do not induce neoplasia but can accelerate tumorigenesis in conjunction with Pten loss (ref: Brown doi.org/10.15252/emmm.202217094/). These findings underscore the complexity of genetic interactions in endometrial cancer and highlight the potential for targeted therapies based on specific molecular profiles. In addition to genetic alterations, the role of tumor suppressor genes such as PTEN and Trp53 has been emphasized, with frequent alterations noted in endometrioid tumors (ref: Mayo doi.org/10.15252/emmm.202318166/). The investigation into primary ovarian endometrioid carcinomas revealed no lymph node metastases in comprehensively staged patients, suggesting a unique spread pattern that may influence treatment strategies (ref: Mazina doi.org/10.1136/ijgc-2023-004627/). Collectively, these studies illustrate the intricate interplay of genetic factors in endometrial carcinoma, paving the way for personalized treatment approaches and improved patient outcomes.