To date, GWAS and transcriptional‐wide association studies (TWAS) have identified numerous genetic risk factors associated with GBM (e.g., EGFR, TP53, FGFR, PTEN, CDKN2A, TERT, TERC) and non‐GBM glioma (e.g., VTI1A, MDM4, AKT3, IDH1, TREH, TERT, TMEM25, PHLDB1).[85, 86, 144, 145, 146] To some extent, such distinction reflects the different etiologies underlying the diseases and also implicates the different druggable gene targets. This evidence concerns the gene VTI1A and glioblastoma.