Research on gliomas, particularly glioblastomas, has revealed significant insights into their biology and the mechanisms driving tumorigenesis. A study highlighted the role of histone H3.3 mutations (G34R/V) in gliomagenesis, showing that these mutations are often found in tumors arising from GSX2/DLX-expressing interneuron progenitors, where they impair neuronal differentiation (ref: Chen doi.org/10.1016/j.cell.2020.11.012/). Another investigation utilized synthetic genetic tracing to map the phenotypic interactions between glioblastoma cells and innate immune cells, shedding light on tumor heterogeneity and resistance to therapy (ref: Schmitt doi.org/10.1158/2159-8290.CD-20-0219/). Furthermore, the integration of glioma cells into tumor microtube-connected networks was identified as a stemness feature, indicating that these networks may contribute to the aggressive nature of gliomas (ref: Xie doi.org/10.1093/neuonc/). The study of microRNA regulation in glioblastoma revealed that aberrant nuclear localization of DICER disrupts microRNA maturation, leading to a down-regulated microRNAome compared to normal brain tissue (ref: Bronisz doi.org/10.1126/sciadv.abc0221/). Collectively, these findings underscore the complexity of glioma biology and the need for targeted therapeutic strategies that consider the tumor microenvironment and genetic landscape.