TNTs, which are composed of F-actin extensions, allow tumor cells to exchange mitochondrial DNA and other critical components, driving tumor repopulation following therapy.185 Additionally, the role of Bruton’s tyrosine kinase (BTK) in GBM core cells suggests that BTK is a potential biomarker for distinguishing intratumor spatial heterogeneity, with implications for targeted therapies.186 The complexity of GBM heterogeneity presents challenges for treatment, necessitating strategies that target multiple tumor subpopulations and their interactions with the microenvironment. This evidence concerns the gene BTK and glioblastoma.