Leiomyosarcoma (LMS) is characterized by distinct genomic alterations that differentiate it from other solid tumors, particularly carcinomas. A study identified that drivers of genomic loss of heterozygosity (gLOH) in LMS are unique, with specific emphasis on alterations in homologous recombination repair genes, notably BRCA2. This research highlights the need for further exploration into the prognostic implications of gLOH in LMS, as its clinical value remains poorly defined (ref: Seligson doi.org/10.1038/s41698-022-00271-x/). Additionally, the role of long non-coding RNA (lncRNA) EGFR-AS1 has been shown to facilitate LMS progression and immune evasion through the EGFR-MYC-PD-L1 axis. The study demonstrated that elevated levels of EGFR-AS1 and PD-L1 correlate negatively with CD8+ T-cell infiltration, suggesting a mechanism by which LMS cells evade immune surveillance (ref: Chen doi.org/10.1093/intimm/). Furthermore, a retrospective analysis of uterine leiomyosarcomas (uLMS) revealed significant frequencies of gene alterations, underscoring the necessity for molecular characterization to identify potential therapeutic targets (ref: Ciccarone doi.org/10.3390/cancers14081934/).