Recent research has significantly advanced our understanding of the molecular mechanisms underlying gliomas, particularly through large-scale genomic studies. The Glioma Longitudinal Analysis (GLASS) consortium has provided insights into the evolutionary characteristics of adult diffuse gliomas by performing temporal DNA sequencing on primary and recurrent glioma pairs, revealing critical molecular events associated with tumor recurrence (ref: Narayanan doi.org/10.1016/j.cell.2020.01.016/). Additionally, a comparative study of canine and human gliomas highlighted the evolutionary conservation of mutational processes, showing that canine gliomas exhibit similarities to human pediatric gliomas in terms of aneuploidy and mutational rates, thereby suggesting a shared tumorigenic mechanism (ref: Amin doi.org/10.1016/j.ccell.2020.01.004/). Furthermore, the identification of SFMBT1 as an oncogenic driver in cancers with VHL loss underscores the importance of targeting specific molecular pathways to develop effective therapies (ref: Liu doi.org/10.1016/j.molcel.2020.01.009/). These findings collectively emphasize the need for a deeper understanding of glioma genetics to inform therapeutic strategies and improve patient outcomes. In addition to genetic insights, the role of long noncoding RNAs (lncRNAs) in glioblastoma treatment resistance has been explored. A study demonstrated that the lncRNA SNHG12 is activated through DNA methylation, promoting temozolomide resistance in glioblastoma, which poses a significant challenge in clinical settings (ref: Lu doi.org/10.1186/s12943-020-1137-5/). This highlights the complex interplay between genetic alterations and epigenetic modifications in glioma progression and treatment resistance. Moreover, the evaluation of depression prevalence using the Patient Health Questionnaire-9 (PHQ-9) in glioma patients revealed discrepancies in estimating actual depression rates, indicating the necessity for more accurate diagnostic tools in this population (ref: Levis doi.org/10.1016/j.jclinepi.2020.02.002/).