In addition, we also found activation and expression of SOX9, E2F4, and KLF10 in Ac-G cluster, which was associated with GBM tumorigenesis, proliferation, and invasion; activation of transcriptive modules (including PRRX2 and HXC9) in Class-G cluster, which was related to immune response regulation [43] and radiotherapy resistance [44]; and activation of CD59 and FOXC2 in Neo-G cluster, which was associated with immunosuppression [45], pathological angiogenesis, and neovascularization [46]. The gene discussed is FOXC2; the disease is glioblastoma.