Seminal studies have established that PN GBMs are characterized by IDH1 mutations, the glioma-CpG island methylator phenotype (G-CIMP+) [58,66], PDGFRA amplification and OLIG2 expression [58,67], whereas MES GBMs are G-CIMP− and share wild-type IDH1, loss of NF1 as well as the expression of CD44, signal transducer and activator of transcription 3 (STAT3) and CCAAT enhancer binding protein beta (CEBPβ) [58,66,68], which finally lead to increased proliferation, resistance to radiation and worse prognosis [69]. Here, CEBPB is linked to glioma.