While the first mutation (EE-019A, chr7:105984983A>T) slightly reduced the affinity of forkhead box protein A1 (FOXA1), increased the affinity of FOXA3, FOXK2, and FOXH1 (Fig. 1F; Fig. S3B, left), the second mutation (EE-019B, chr7:105985025G>A) increased the affinity of STAT3 and Thanatos-associated protein domain-containing 1 (THAP1), TFs involved in GBM proliferation and immune evasion. This evidence concerns the gene FOXA1 and glioblastoma.