Molecularly, GBM exhibits distinct subtypes based on key genetic alterations, such as IDH mutations, H3K27 alterations (e.g., H3K27me3 loss due to EZH2 dysfunction), as well as mutations in H3F3A leading to H3K27M oncogenic transformation (Sturm et al., 2012), EGFR amplification, and TERT promoter mutations, each contributing to diverse tumor behaviors and therapeutic responses (Chai et al., 2024; Hadad et al., 2023). Here, EZH2 is linked to neoplasm.