E2F1 and glioblastoma: Computational modeling demonstrated that these SNVs disrupted transcription factor (TF) binding motifs, altering the affinity of key TFs, such as transcriptional enhancer-associated domain (TEAD), early 2 factor 1 (E2F1), and signal transducer and activator of transcription 3 (STAT3), which are known to drive GBM malignancy.